All Phenotypes Ptgs2<tm1Unc> MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Ptgs2^tm1Unc
targeted mutation 1, University of North Carolina
MGI:2158457

Summary

23 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Ptgs2^tm1Unc/Ptgs2^tm1Unc	B6.129P2-Ptgs2^tm1Unc	MGI:4366271
hm2	Ptgs2^tm1Unc/Ptgs2^tm1Unc	B6;129P2-Ptgs2^tm1Unc/Tac	MGI:4366285
hm3	Ptgs2^tm1Unc/Ptgs2^tm1Unc	D1.129P2(B6J)-Ptgs2^tm1Unc	MGI:3603831
hm4	Ptgs2^tm1Unc/Ptgs2^tm1Unc	D1.129P2-Ptgs2^tm1Unc	MGI:4366267
hm5	Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd	MGI:4366244
hm6	Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6	MGI:4366263
hm7	Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6 * DBA/1	MGI:4366277
hm8	Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:2177811
hm9	Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129/Sv * 129P2/OlaHsd * C57BL/6	MGI:4366241
ht10	Ptgs2^tm1Unc/Ptgs2⁺	B6.129P2-Ptgs2^tm1Unc	MGI:4366272
ht11	Ptgs2^tm1Unc/Ptgs2⁺	D1.129P2(B6J)-Ptgs2^tm1Unc	MGI:3603834
ht12	Ptgs2^tm1Unc/Ptgs2⁺	D1.129P2-Ptgs2^tm1Unc	MGI:4366266
ht13	Ptgs2^tm1Unc/Ptgs2⁺	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366164
ht14	Ptgs2^tm1Unc/Ptgs2⁺	involves: 129/Sv * 129P2/OlaHsd * C57BL/6	MGI:4366242
ht15	Ptgs2^tm1Unc/Ptgs2^tm2.1Hahe	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:4440882
cx16	Ptgs1^tm1Unc/Ptgs1^tm1Unc Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6 * CD-1	MGI:3812358
cx17	Ptgs1^tm1Unc/Ptgs1^tm1Unc Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:3812381
cx18	Ptgs1^tm1Unc/Ptgs1⁺ Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:3812383
cx19	Ptgs1^tm1Unc/Ptgs1⁺ Ptgs2^tm1Unc/Ptgs2⁺	involves: 129P2/OlaHsd * C57BL/6J	MGI:3812385
cx20	Ptgs1^tm1Unc/Ptgs1^tm1Unc Ptgs2^tm1Unc/Ptgs2⁺	involves: 129P2/OlaHsd * C57BL/6J	MGI:3812386
cx21	Apc^Min/Apc⁺ Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366246
cx22	Hr^hr/Hr^hr Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6 * SKH1	MGI:4366347
cx23	Hr^hr/Hr^hr Ptgs2^tm1Unc/Ptgs2⁺	involves: 129P2/OlaHsd * C57BL/6 * SKH1	MGI:4366348

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	B6.129P2-Ptgs2^tm1Unc

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

abnormal class switch recombination ( J:140698 )

• 21 days post-vaccination with HPV, mice exhibit 34% fewer B220+IgG1+ and 50% fewer B220+Ig2a+ cells compared to in wild-type mice

• however, IgG2b and IgG3 class switching is normal

abnormal memory B cell differentiation ( J:140698 )

• mice vaccinated with HPV-like particles exhibit reduced spleen memory B cell expansion compared with similarly treated wild-type mice

decreased IgG1 level ( J:140698 )

• 69% in mice vaccinated with HPV-like particles

decreased IgG2a level ( J:140698 )

• 89% in mice vaccinated with HPV-like particles

decreased IgG3 level ( J:140698 )

• 43% in mice vaccinated with HPV-like particles

increased IgM level ( J:140698 )

• 4-fold in mice vaccinated with HPV-like particles

decreased susceptibility to induced arthritis ( J:110716 )

• FCA-treated female mice exhibit reduced joint destruction compared with similarly treated male wild-type mice

abnormal response to infection ( J:140698 )

• mice vaccinated with HPV-like particles produce 70% fewer viral-like particle antibodies and 80% fewer viral-like particle antibody-secreting cells compared with similarly treated wild-type mice

• mice vaccinated with HPV-like particles produce more IgM and fewer IgG1 (69%), IgG2a (89%), and IgG3 (43%) antibodies compared to in similarly treated wild-type mice

• mice vaccinated with HPV-like particles produce more IgM producing cells and fewer IgG1 (78%), IgG2a (70%), IgG2b (15%), and IgG3 (55%) secreting cells compared with similarly treated wild-type mice

• mice vaccinated with HPV-like particles produce 10-fold fewer virus like particle-specific neutralizing antibodies compared to in similarly treated wild-type mice

• mice vaccinated with HPV-like particles exhibit reduced spleen memory B cell expansion compared with similarly treated wild-type mice

cardiovascular system

abnormal choriocapillaris morphology ( J:281382 )

• at 12 months of age, vascular corrosion casts of homozygous mice are extremely brittle and show a moth-eaten appearance secondary to capillary dropout as detected by the increased avascular area

• severe involution of the choriocapillaris at 12 months of age shown by significant reduction in capillary thickness

• homozygous mice did not develop degeneration of photoreceptors by 12 mo of age

vision/eye

abnormal choriocapillaris morphology ( J:281382 )

• at 12 months of age, vascular corrosion casts of homozygous mice are extremely brittle and show a moth-eaten appearance secondary to capillary dropout as detected by the increased avascular area

• severe involution of the choriocapillaris at 12 months of age shown by significant reduction in capillary thickness

• homozygous mice did not develop degeneration of photoreceptors by 12 mo of age

homeostasis/metabolism

decreased susceptibility to neuronal excitotoxicity ( J:67211 )

• mice exhibit reduced NMDA-induced damage compared to in wild-type mice

decreased prostaglandin level ( J:67211 )

• following occlusion of the middle cerebral artery, mice fail to exhibit an increase in cortical prostaglandin unlike similarly treated wild-type mice

abnormal response/metabolism to endogenous compounds ( J:125586 )

• after 90 to 120 minutes, IL1beta-fed mice exhibit a reduced decrease in drinking behavior compared with similarly treated wild-type mice

• however, IL1beta-fed mice exhibit a normal decrease in drinking behavior after 30 minutes

abnormal response to CNS ischemic injury ( J:67211 )

• following occlusion of the middle cerebral artery, mice fail to exhibit an increase in cortical prostaglandin unlike similarly treated wild-type mice

decreased cerebral infarct size ( J:67211 )

• 96 hours after occlusion of the middle cerebral artery, infarct size is reduced 34% compared to in similarly treated wild-type mice

• 96 hours after occlusion of the middle cerebral artery, infarct size is reduced 38% compared to in similarly treated wild-type mice

nervous system

decreased susceptibility to neuronal excitotoxicity ( J:67211 )

• mice exhibit reduced NMDA-induced damage compared to in wild-type mice

abnormal response to CNS ischemic injury ( J:67211 )

• following occlusion of the middle cerebral artery, mice fail to exhibit an increase in cortical prostaglandin unlike similarly treated wild-type mice

decreased cerebral infarct size ( J:67211 )

• 96 hours after occlusion of the middle cerebral artery, infarct size is reduced 34% compared to in similarly treated wild-type mice

• 96 hours after occlusion of the middle cerebral artery, infarct size is reduced 38% compared to in similarly treated wild-type mice

behavior/neurological

abnormal drinking behavior ( J:125586 )

• after 90 to 120 minutes, IL1beta-fed mice exhibit a reduced decrease in drinking behavior compared with similarly treated wild-type mice

• however, IL1beta-fed mice exhibit a normal decrease in drinking behavior after 30 minutes

abnormal nociception after inflammation ( J:110716 )

• FCA-treated mice fail to develop ipsilateral and contralateral mechanical allodynia unlike similarly treated wild-type mice

• FCA-treated mice fail to develop thermal hyperalgesia unlike similarly treated wild-type mice

allodynia ( J:110716 )

• FCA-treated mice fail to develop ipsilateral and contralateral mechanical allodynia unlike similarly treated wild-type mice

increased thermal nociceptive threshold ( J:110716 )

• FCA-treated mice fail to develop thermal hyperalgesia unlike similarly treated wild-type mice

skeleton

decreased susceptibility to induced arthritis ( J:110716 )

• FCA-treated female mice exhibit reduced joint destruction compared with similarly treated male wild-type mice

hematopoietic system

abnormal class switch recombination ( J:140698 )

• 21 days post-vaccination with HPV, mice exhibit 34% fewer B220+IgG1+ and 50% fewer B220+Ig2a+ cells compared to in wild-type mice

• however, IgG2b and IgG3 class switching is normal

abnormal memory B cell differentiation ( J:140698 )

• mice vaccinated with HPV-like particles exhibit reduced spleen memory B cell expansion compared with similarly treated wild-type mice

decreased IgG1 level ( J:140698 )

• 69% in mice vaccinated with HPV-like particles

decreased IgG2a level ( J:140698 )

• 89% in mice vaccinated with HPV-like particles

decreased IgG3 level ( J:140698 )

• 43% in mice vaccinated with HPV-like particles

increased IgM level ( J:140698 )

• 4-fold in mice vaccinated with HPV-like particles

cellular

decreased susceptibility to neuronal excitotoxicity ( J:67211 )

• mice exhibit reduced NMDA-induced damage compared to in wild-type mice

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	B6;129P2-Ptgs2^tm1Unc/Tac

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Hypertoprhy of glomeruli in Ptgs2^tm1Unc/Ptgs2^tm1Unc mice that is not seen in Ptgs2^tm1.1Wls/Ptgs2^tm1.1Wls mice

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:141610 )

• 3 of 18 kainate-treated mice die unlike similarly treated wild-type mice

• kainate-treated mice pretreated with the CB1 antagonist, AM-251, exhibit increased mortality compared with similarly treated wild-type mice

renal/urinary system

renal glomerulus hypertrophy ( J:156331 )

nervous system

increased susceptibility to pharmacologically induced seizures ( J:141610 )

• kainate-treated mice exhibit increased Racine seizure score, neuronal damage, and mortality compared with similarly treated wild-type mice

• pretreatment with the CB1 antagonist, AM-251, increases seizure intensity, neuronal damage, and mortality in kainate-treated mice unlike in similarly treated wild-type mice

tonic-clonic seizures ( J:141610 )

• 5 of 18 kainate-treated mice reach maximal seizure intensity that includes tonic-clonic seizures unlike in similarly treated wild-type mice

increased susceptibility to neuronal excitotoxicity ( J:141610 )

• kainate-treated mice exhibit increased Racine seizure score, neuronal damage, and mortality compared with similarly treated wild-type mice

abnormal inhibitory postsynaptic currents ( J:141610 )

• the frequency of spontaneous inhibitory postsynaptic current is decreased 61% compared to in wild-type mice

homeostasis/metabolism

increased susceptibility to neuronal excitotoxicity ( J:141610 )

• kainate-treated mice exhibit increased Racine seizure score, neuronal damage, and mortality compared with similarly treated wild-type mice

decreased prostaglandin level ( J:141610 )

• in the brain

increased susceptibility to xenobiotic induced morbidity/mortality ( J:141610 )

• 3 of 18 kainate-treated mice die unlike similarly treated wild-type mice

• kainate-treated mice pretreated with the CB1 antagonist, AM-251, exhibit increased mortality compared with similarly treated wild-type mice

abnormal response to injury ( J:107751 )

• following muscle injury, mice exhibit reduced inflammation compared with similarly treated wild-type mice

abnormal bone healing ( J:112346 )

• healing bone fractures exhibit little or no callus with reduced bone formation and decreased endochondral ossification compared to in wild-type mice

skeleton

abnormal bone healing ( J:112346 )

• healing bone fractures exhibit little or no callus with reduced bone formation and decreased endochondral ossification compared to in wild-type mice

abnormal endochondral bone ossification ( J:112346 )

• bone fractures exhibit little to no endochondral bone ossification unlike in similarly treated wild-type mice

muscle

impaired skeletal muscle regeneration ( J:107751 )

• following muscle injury, mice exhibit reduced muscle regeneration and 31% smaller regenerating myofibers compared with wild-type mice

behavior/neurological

increased susceptibility to pharmacologically induced seizures ( J:141610 )

• kainate-treated mice exhibit increased Racine seizure score, neuronal damage, and mortality compared with similarly treated wild-type mice

• pretreatment with the CB1 antagonist, AM-251, increases seizure intensity, neuronal damage, and mortality in kainate-treated mice unlike in similarly treated wild-type mice

tonic-clonic seizures ( J:141610 )

• 5 of 18 kainate-treated mice reach maximal seizure intensity that includes tonic-clonic seizures unlike in similarly treated wild-type mice

cellular

increased susceptibility to neuronal excitotoxicity ( J:141610 )

• kainate-treated mice exhibit increased Racine seizure score, neuronal damage, and mortality compared with similarly treated wild-type mice

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	D1.129P2(B6J)-Ptgs2^tm1Unc

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

mortality/aging ( J:64383 )

N	• Background Sensitivity: adult homozygotes do not exhibit reduced longevity, unlike homozygotes generated on a predominantly C57BL/6J background

postnatal lethality ( J:102777 )

• only 66% of homozygotes survive to weaning versus 92% of wild-type controls; however, no adult mice are found to die spontaneously during a 6-month study period

• Background Sensitivity: adult homozygotes do not die from renal failure, unlike homozygotes generated on a predominantly C57BL/6 background

renal/urinary system

abnormal kidney morphology ( J:64383 )

• Background Sensitivity: adult homozygotes do not exhibit the severe renal pathology observed in homozygotes of a predominantly C57BL/6J genetic background

renal glomerulus cyst ( J:102777 )

• by 9 months of age, small subcapsular glomeruli are detected in cystic spaces

• Background Sensitivity: cystic changes are less severe than those observed on a predominantly C57BL/6 background

abnormal renal glomerulus morphology ( J:102777 )

• hypoplastic subcapsular glomeruli are observed by P14 and become cystic as mice age, unlike in wild-type controls

renal glomerulus hypertrophy ( J:102777 )

• inner cortical hyperplastic glomeruli are seen at 3 weeks of age, unlike in wild-type controls

abnormal kidney mesenchyme morphology ( J:102777 )

• undifferentiated mesenchyme is seen as early as P7, unlike in wild-type controls

renal interstitial fibrosis ( J:102777 )

• interstitial fibrosis is noted at 3 weeks and becomes prominent by 8 months of age

small kidney ( J:102777 )

• mutant kidneys are smaller than wild-type

decreased kidney weight ( J:102777 )

• at 34 weeks of age, the ratio of kidney weight to total body weight is significantly lower than that of wild-type controls

granular kidney ( J:102777 )

• mutant kidneys have a more granular surface than wild-type

pale kidney ( J:102777 )

• mutant kidneys appear paler than wild-type

reproductive system

female infertility ( J:64383 )

• female homozygous mutant mice are infertile

homeostasis/metabolism

increased circulating creatinine level ( J:102777 )

• at 10, 16, 20 and 28 weeks of age, average plasma creatinine levels are significantly higher than in wild-type controls

increased blood urea nitrogen level ( J:102777 )

• at 2-8 months of age, homozygotes show a ~2-fold increase in BUN levels relative to wild-type controls

• Background Sensitivity: increase in BUN levels is significantly lower than that reported for homozygotes on a B6 genetic background (200% versus 270%)

hematopoietic system

decreased hematocrit ( J:102777 )

• hematocrit values are significantly lower than those of wild type controls at most time points during a 6-month study period

behavior/neurological

behavior/neurological phenotype ( J:64383 )

N	• both male and female homozygotes display normal reaction times in the hot plate test, indicating normal thermal nociception

decreased aggression ( J:64383 )

• homozygotes appear to be less excitable and easier to handle than wild-type littermates

• docile behavior is most evident in female homozygotes

growth/size/body

renal glomerulus cyst ( J:102777 )

• by 9 months of age, small subcapsular glomeruli are detected in cystic spaces

• Background Sensitivity: cystic changes are less severe than those observed on a predominantly C57BL/6 background

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	D1.129P2-Ptgs2^tm1Unc

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

decreased prostaglandin level ( J:102779 )

• fat pad tissue from mice fed a high fat and sucrose diet exhibit a 20% decrease in prostaglandin production compared with tissues from similarly treated wild-type mice

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

digestive/alimentary system

digestive/alimentary phenotype ( J:108679 )

N	• mice exhibit normal radiation-induced crypt epithelial cell apoptosis

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:60668 , J:158426 )

• following treatment with a high dose of DSS, survival is decreased by day 4 and drops to 50% by day 5 whereas similarly treated wild-type mice do not exhibit any decrease in survival (J:60668)

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice (J:158426)

premature death ( J:104002 )

• about 20% of mice die between 7 and 23 weeks of age

immune system

increased susceptibility to induced colitis ( J:60668 , J:158426 )

• mice treated with a high dose of DSS exhibit increased weight loss, intestinal inflammation score, and mortality compared with similarly treated wild-type mice (J:60668)

• DSS-treated mice fail to exhibit an increase in colonic secretion of prostaglandin unlike similarly treated wild-type mice (J:60668)

• mice treated with a low dose of DSS exhibit increased clinical inflammation and weight lose compared with similarly treated wild-type mice (J:60668)

• DSS-treated mice exhibit increased colonic shortening, colonic weight to length ratio, splenomegaly, white blood cell counts, and crypt damage and decreased hematocrit compared with similarly treated wild-type mice (J:60668)

• DSS-treated mice exhibit a more aggressive mucosal injury than in similarly treated wild-type mice and Ptgs1^tm1Unc homozygotes (J:60668)

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice (J:158426)

peritoneal inflammation ( J:60668 )

• in 2 of 10 mice unlike wild-type mice

enlarged spleen ( J:60668 )

• in DSS-treated mice compared with similarly treated wild-type mice

increased leukocyte cell number ( J:60668 )

• in DSS-treated mice compared with similarly treated wild-type mice

increased tumor necrosis factor secretion ( J:108054 )

• in the pancreas and bronchoalveolar lavage fluid of cerulein-treated mice compared with similarly treated wild-type mice

decreased susceptibility to endotoxin shock ( J:75611 )

• LPS-treated mice exhibit less weight loss than similarly treated wild-type mice

digestive/alimentary system

abnormal colon morphology ( J:60668 )

• DSS-treated mice exhibit increased colonic shortening and colonic weight to length ratio compared with similarly treated wild-type mice

increased susceptibility to induced colitis ( J:60668 , J:158426 )

• mice treated with a high dose of DSS exhibit increased weight loss, intestinal inflammation score, and mortality compared with similarly treated wild-type mice (J:60668)

• DSS-treated mice fail to exhibit an increase in colonic secretion of prostaglandin unlike similarly treated wild-type mice (J:60668)

• mice treated with a low dose of DSS exhibit increased clinical inflammation and weight lose compared with similarly treated wild-type mice (J:60668)

• DSS-treated mice exhibit a more aggressive mucosal injury than in similarly treated wild-type mice and Ptgs1^tm1Unc homozygotes (J:60668)

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice (J:158426)

peritoneal inflammation ( J:60668 )

• in 2 of 10 mice unlike wild-type mice

growth/size/body

growth/size/body region phenotype ( J:104002 )

N	• mice display normal somatic growth from birth to 42 days of age

increased heart weight ( J:104002 )

• at birth, mice exhibit a significantly higher heart weight:body weight ratio relative to control mice

• however, a normal ratio is observed during postnatal growth and early adulthood

weight loss ( J:60668 )

• compared with wild-type mice when treated with a high or low dose of DSS

kidney cyst ( J:104002 )

• early cystic changes affecting different tubule sections and glomeruli at P10, with slightly variable pathologic progression

• severe cyst formation by P28

kidney cortex cyst ( J:104002 )

• massive tubular cysts in severely affected kidneys at P14

renal glomerulus cyst ( J:104002 )

• by P14, all mice exhibit cystic subcapsular glomeruli

enlarged spleen ( J:60668 )

• in DSS-treated mice compared with similarly treated wild-type mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:104002 )

N	• adult mice exhibit normal plasma sodium, potassium, bicarbonate and chloride levels relative to wild-type controls

abnormal response of heart to induced stress ( J:103388 )

• following ischemia, maximum contracture is higher and recovery of contractile function is lower than in similarly treated wild-type mice

• however, pre-conditioned mice exhibit normal recovery from myocardial ischemia

increased circulating creatinine level ( J:104002 )

• adult mice exhibit a 1.5-fold increase in plasma creatinine levels relative to controls

increased blood urea nitrogen level ( J:104002 )

• adult mice exhibit a 2.5-fold increase in plasma BUN levels relative to controls

abnormal enzyme/coenzyme level ( J:108054 )

• cerulein-treated mice exhibit reduced pancreatic and lung myeloperoxidase levels compared with similarly treated wild-type mice

decreased lactate dehydrogenase level ( J:108054 )

• in the bronchoalvealor lavage fluid of cerulein-treated mice compared with similarly treated wild-type mice

decreased prostaglandin level ( J:60668 , J:117986 )

• DSS-treated mice fail to exhibit an increase in colonic secretion of prostaglandin unlike similarly treated wild-type mice (J:60668)

• in keratinocyte cultures (J:117986)

increased susceptibility to xenobiotic induced morbidity/mortality ( J:60668 , J:158426 )

• following treatment with a high dose of DSS, survival is decreased by day 4 and drops to 50% by day 5 whereas similarly treated wild-type mice do not exhibit any decrease in survival (J:60668)

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice (J:158426)

decreased incidence of tumors by chemical induction ( J:158426 )

• mice treated with azoxymethane alone fail to develop colon tumors unlike similarly treated wild-type mice

decreased susceptibility to injury ( J:108054 )

• cerulein-treated mice exhibit less pancreatitis-associated lung injury compared with similarly treated wild-type mice

hematopoietic system

enlarged spleen ( J:60668 )

• in DSS-treated mice compared with similarly treated wild-type mice

anemia ( J:60668 )

• DSS-treated mice exhibit reduced hematocrit compared with similarly treated wild-type mice

decreased hematocrit ( J:60668 )

• DSS-treated mice exhibit reduced hematocrit compared with similarly treated wild-type mice

increased leukocyte cell number ( J:60668 )

• in DSS-treated mice compared with similarly treated wild-type mice

cardiovascular system

cardiovascular system phenotype ( J:104002 )

N	• normal systolic blood pressure in awake or anesthetized mice relative to wild-type controls

increased heart weight ( J:104002 )

• at birth, mice exhibit a significantly higher heart weight:body weight ratio relative to control mice

• however, a normal ratio is observed during postnatal growth and early adulthood

abnormal response of heart to induced stress ( J:103388 )

• following ischemia, maximum contracture is higher and recovery of contractile function is lower than in similarly treated wild-type mice

• however, pre-conditioned mice exhibit normal recovery from myocardial ischemia

muscle

muscle phenotype ( J:146321 )

N	• mice exhibit normal internal anal sphincter muscle tone

endocrine/exocrine glands

pancreas necrosis ( J:108054 )

• in cerulein-treated mice compared with similarly treated wild-type mice

decreased susceptibility to induced pancreatitis ( J:108054 )

• following supramaximally stimulating doses of cerulein, mice develop decreased pancreatitis and associated lung injury with reduced , acinar cell necrosis, pancreatic and lung myeloperoxidase activity, bronchoalveolar lavage (BAL) fluid lactate dehydrogenase levels, and pancreatic and BAL TNF-alpha levels compared with similarly treated wild-type mice

neoplasm

decreased incidence of tumors by chemical induction ( J:158426 )

• mice treated with azoxymethane alone fail to develop colon tumors unlike similarly treated wild-type mice

increased incidence of induced tumors ( J:158426 )

• mice treated with azoxymethane and dextran sulfate sodium exhibit more colon tumors than similarly treated wild-type mice

• however, the histology of induced-tumors is the same as in similarly treated wild-type mice

integument

abnormal keratinocyte differentiation ( J:117986 )

• keratinocyte cultures exhibit a 5-fold increase in expression of K1, a marker of differentiation, compared with wild-type cells

cellular

pancreas necrosis ( J:108054 )

• in cerulein-treated mice compared with similarly treated wild-type mice

abnormal keratinocyte differentiation ( J:117986 )

• keratinocyte cultures exhibit a 5-fold increase in expression of K1, a marker of differentiation, compared with wild-type cells

renal/urinary system

renal/urinary system phenotype ( J:104002 )

N	• adult mice exhibit normal urinalysis and 24-hr urine output under non-stressed conditions • no significant differences in urine osmolarity or in daily urinary excretion of sodium, potassium and chloride are observed

kidney cyst ( J:104002 )

• early cystic changes affecting different tubule sections and glomeruli at P10, with slightly variable pathologic progression

• severe cyst formation by P28

kidney cortex cyst ( J:104002 )

• massive tubular cysts in severely affected kidneys at P14

renal glomerulus cyst ( J:104002 )

• by P14, all mice exhibit cystic subcapsular glomeruli

abnormal kidney cortex morphology ( J:104002 )

• by P14, all mice exhibit outer cortical dysplasia

• inner cortical nephron hypertrophy by P42

abnormal renal glomerulus morphology ( J:104002 )

• small, crowded glomeruli in subcapsular region at P10

• outer cortical glomerular hypoplasia at P42

glomerulosclerosis ( J:104002 )

• focally variable glomerular sclerosis by P42

• however, no inflammatory infiltrate or vascular pathology is observed at any stage

renal glomerulus fibrosis ( J:104002 )

• peri-glomerular fibrosis by P42

renal glomerulus hypertrophy ( J:104002 )

• hypertrophy of juxtamedullary glomeruli at P28

• inner cortical glomerular hypertrophy by P42

abnormal kidney development ( J:104002 )

• mice exhibit progressive cystic dysplasia during the later stages of kidney development

• however, prenatal and early postnatal kidney development appears normal

renal interstitial fibrosis ( J:104002 )

• diffuse interstitial fibrosis by P42

decreased kidney weight ( J:104002 )

• starting at P10, total kidney mass is significantly reduced relative to that in wild-type controls

• kidney-specific growth suppression persists to P42 with no significant change

renal tubule atrophy ( J:104002 )

• by P14, all mice exhibit loss of proximal tubular mass

abnormal proximal convoluted tubule morphology ( J:104002 )

• variable loss of normal proximal tubule mantle at P10

proximal convoluted tubule brush border loss ( J:104002 )

• by P14, all mice exhibit loss of brush border definition

dilated renal tubule ( J:104002 )

• variable tubular dilation at P10

• severe diffuse tubular dilation by P42

renal tubule hypertrophy ( J:104002 )

• hypertrophy of juxtamedullary tubules by P28

kidney degeneration ( J:104002 )

• at 8 weeks of age, some mice exhibit more severe cystic degeneration than others

decreased renal glomerular filtration rate ( J:104002 )

• adult mice exhibit a ~50% reduction in GFR relative to wild-type controls, as measured by inulin clearance

kidney failure ( J:104002 )

• mice exhibit progressive renal insufficiency

behavior/neurological

behavior/neurological phenotype ( J:104002 )

N	• mice exhibit normal daily water intake under non-stressed conditions

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * DBA/1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

abnormal wound healing ( J:126734 )

• the tensile strength of skin at the site of wound healing is 70% less than in similarly treated wild-type mice

• 8 days after wounding, endothelial cell staining at the site of the wound is increased 70% compared to in similarly treated wild-type mice

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

spleen hyperplasia ( J:29510 )

• homozygotes with peritonitis exhibit myeloid hyperplasia in their spleen

mortality/aging

decreased survivor rate ( J:67208 )

• mice that survive the postnatal period survive weaning

premature death ( J:29510 )

• several mice die at ~8 weeks of age

neonatal lethality, incomplete penetrance ( J:67208 )

• 35% of mice die within the first 24 to 48 hrs of birth

postnatal lethality, incomplete penetrance ( J:67208 )

• 35% of mice die within the first 24 to 48 hrs of birth

reproductive system

abnormal corpus luteum morphology ( J:55145 )

• at 24-36 hrs after hCG treatment, PMSG-primed mutant ovaries display formation of corpora hemorrhagica but oocytes remain in the antral cavity without exophytic, cellular ovulation sites around stigmata

abnormal cumulus expansion ( J:55145 )

• at 8 hrs after hCG treatment, PMSG-primed homozygotes exhibit attenuated or unorganized cumulus expansion, despite evidence of oocyte activation (i.e. germinal vesicle breakdown and resumption of meiosis)

abnormal reproductive system physiology ( J:29510 )

• matings between F1 heterozygotes result in abnormal Mendelian ratios of male F2 progeny (28:20:12), whereas genotype ratios of female progeny are normal (15:31:11)

• however, equal numbers of males (60) and females (56) reach weaning age, despite differences in genotype ratios of male and female weanlings, suggesting a possible pre-implantation defect

impaired granulosa cell differentiation ( J:55145 )

• at 8 hrs after hCG treatment, PMSG-primed homozygotes exhibit lack of organized cumulus granulosa cell polarization or expansion

decreased superovulation rate ( J:55145 )

• at 24-30 hrs after hCG treatment, only 2 of nine PMSG-primed homozygotes ovulate, with only 2 or 3 isolated oocytes without cumulus mass

failure of superovulation ( J:55145 )

• at 24-30 hrs after hCG treatment, 7 of nine PMSG-primed homozygotes exhibit absence of oocytes and cumulus mass in their oviducts

• ovulation is restored upon gonadotropin stimulation and simultaneous treatment with PGE2 or interleukin-1beta; treatment with PGF2alpha is less effective

female infertility ( J:55145 )

• female homozygotes exhibit estrous cyclicity and normal copulation but fail to impregnate and deliver viable pups, even after PMSG/hCG stimulation

renal/urinary system

tubulointerstitial nephritis ( J:29510 )

• nephropathy is often associated with tubular dilation and interstitial inflammation

abnormal kidney morphology ( J:29510 )

• abnormal renal pathology is first noted at ~6 weeks and progresses with increasing age; males are more severely affected than females

• all adult homozygotes show renal lesions of mild to marked severity

• however, normal renal histology, with a normal subcapsular (immature) nephrogenic zone and normal numbers of glomeruli are observed in the renal cortex at 3 weeks of age

abnormal kidney capsule morphology ( J:29510 )

• by 8 weeks, mutant kidneys appear granular on the capsular surface

glomerulosclerosis ( J:29510 )

• at 16 weeks, a single male survivor displays focal segmental and global glomerulosclerosis

• however, renal arteries and arterioles appear normal

decreased renal glomerulus number ( J:29510 )

• at 6 weeks, abnormally low numbers of glomeruli are observed in the renal cortex

renal glomerulus hypertrophy ( J:29510 )

• subcapsular glomerular hypoplasia occurs in conjunction with hypertrophy of deeper cortical glomeruli

abnormal kidney development ( J:29510 )

• homozygotes exhibit a postnatal maturation arrest in the subcapsular nephrogenic zone

abnormal nephrogenic zone morphology ( J:29510 )

• homozygotes exhibit a postnatal maturation arrest in the subcapsular nephrogenic zone

renal interstitial fibrosis ( J:29510 )

• at 8 weeks, affected kidneys show a few small scattered foci of interstitial fibrosis, not seen at 6 weeks of age

• at 16 weeks, a single male survivor displays severe focal interstitial fibrosis

abnormal kidney papilla morphology ( J:29510 )

• nephropathy is often associated with papillary mineralization

small kidney ( J:29510 )

• at 8 weeks, mutant kidneys are small

kidney cortex atrophy ( J:29510 )

• in some cases, the kidney cortex appears thinned

renal tubule atrophy ( J:29510 )

• at 8 weeks, affected kidneys show a few small scattered foci of tubular atrophy, not seen at 6 weeks of age

• at 16 weeks, a single male survivor displays severe tubular atrophy

decreased nephron number ( J:29510 )

• in mild cases, nephron hypoplasia in the subcapsular region is characterized by small immature glomeruli and tubules

dilated renal tubule ( J:29510 )

• nephropathy is often associated with tubular dilation

renal cast ( J:29510 )

• nephropathy is often associated with protein and cellular casts in the tubular lumens

nephrocalcinosis ( J:29510 )

• nephropathy is often associated with papillary mineralization

pale kidney ( J:29510 , J:55145 )

• at 8 weeks, mutant kidneys are pale (J:29510)

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:55145 )

N	• PMSG-primed homozygotes display normal serum estradiol levels and normal serum progesterone levels at 8 and 24 hrs after hCG treatment, respectively

intestinal edema ( J:29510 )

• at 8 weeks, homozygotes with peritonitis exhibit submucosal edema of the bowel wall

increased circulating follicle stimulating hormone level ( J:55145 )

• homozygotes exhibit significantly increased pituitary FSH contents relative to wild-type mice

• in addition, homozygotes tend to exhibit higher serum FSH values relative to wild-type mice

increased circulating luteinizing hormone level ( J:55145 )

• homozygotes tend to exhibit increased pituitary LH levels relative to wild-type mice

• in contrast, mutants show no significant changes in hypothalamic tissue levels of gonadotropin releasing hormone 1 (GNRH1; also, LHRH)

abnormal thrombosis ( J:109021 )

• hypoxia-treated mice exhibit increased fibrin and platelet depositions in retinal vessels compared to in similarly treated wild-type retinas

impaired febrile response ( J:54450 )

• LPS-treated mice fail to exhibit an increase in core body temperature unlike similarly treated wild-type mice

abnormal lipid homeostasis ( J:121680 )

• brains contain 15% more phosphatidylserine and 37%, 27%, and 32% less triacylglycerol and cholesterol concentrations and cholesterol-to-phospholipid ratio, respectively, than in wild-type brains

decreased prostaglandin level ( J:55145 , J:109021 )

• at 48 hrs after PMSG treatment, homozygotes show reduced PGE2 levels relative to wild-type mice (J:55145)

• at 8 hrs after hCG treatment, PMSG-primed wild-type ovaries exhibit a 4-fold increase in PGE2 contents, whereas PGE2 values remain unchanged in mutant ovaries (J:55145)

• in the retina (J:109021)

cardiovascular system

abnormal induced retina neovascularization ( J:109021 )

• following hypoxia-treatment, the area of retinal nonperfusion is increased compared to in similarly treated wild-type retinas

patent ductus arteriosus ( J:67208 )

• 33% of mice that die within the first 48 hrs of birth exhibit patent ductus arteriosus

• unlike in wild type mice, treatment with indomethacin does not induce premature closure of the ductus arteriosus and associated neonatal lethality

increased systemic arterial blood pressure ( J:155373 )

• basal blood pressure is greater than in wild-type mice

increased systemic arterial diastolic blood pressure ( J:155373 )

• during the inactive day and active night, mice exhibit increased diastolic blood pressure compared with wild-type mice

• however, stress induced changes in blood pressure are normal

increased systemic arterial systolic blood pressure ( J:155373 )

• during the inactive day and active night, mice exhibit increased systolic blood pressure compared with wild-type mice

• however, stress induced changes in blood pressure are normal

immune system

immune system phenotype ( J:29510 )

N	• homozygotes display normal inflammatory responses to treatments with TPA or arachidonic acid, as measured by ear thickness

peritoneal inflammation ( J:29510 )

• 2 of 7 homozygotes examined at ~8 weeks exhibit suppurative peritonitis

• suppurative peritonitis is acute in male homozygotes and chronic in female homozygotes

• in affected males, peritonitis involves multiple abdominal organs and is typified by purulent exudate, focal acute inflammation of the muscularis, and focal accumulation of rod-like bacteria

• at 8 weeks, homozygotes with peritonitis exhibit multiple fibrinous adhesions among the abdominal organs

spleen hyperplasia ( J:29510 )

• homozygotes with peritonitis exhibit myeloid hyperplasia in their spleen

abnormal macrophage physiology ( J:29510 )

• in culture, homozygous mutant peritoneal macrophages fail to exhibit LPS induction of PGE2 synthesis

abnormal mesenteric lymph node morphology ( J:29510 )

• homozygous females with peritonitis show significant lymphoplasmacytic hyperplasia of the mesenteric lymph node

tubulointerstitial nephritis ( J:29510 )

• nephropathy is often associated with tubular dilation and interstitial inflammation

digestive/alimentary system

abnormal intestinal mucosa morphology ( J:29510 )

• at 8 weeks, homozygotes with peritonitis exhibit submucosal edema of the bowel wall, associated with a prominent neutrophilic infiltrate and leukocytoclasia (necrosis)

• in affected females, abscesses and chronic inflammatory tissue between lobes of the liver and loops of the bowel are observed

intestinal edema ( J:29510 )

• at 8 weeks, homozygotes with peritonitis exhibit submucosal edema of the bowel wall

peritoneal inflammation ( J:29510 )

• 2 of 7 homozygotes examined at ~8 weeks exhibit suppurative peritonitis

• suppurative peritonitis is acute in male homozygotes and chronic in female homozygotes

• in affected males, peritonitis involves multiple abdominal organs and is typified by purulent exudate, focal acute inflammation of the muscularis, and focal accumulation of rod-like bacteria

• at 8 weeks, homozygotes with peritonitis exhibit multiple fibrinous adhesions among the abdominal organs

endocrine/exocrine glands

impaired granulosa cell differentiation ( J:55145 )

• at 8 hrs after hCG treatment, PMSG-primed homozygotes exhibit lack of organized cumulus granulosa cell polarization or expansion

abnormal corpus luteum morphology ( J:55145 )

abnormal cumulus expansion ( J:55145 )

hematopoietic system

spleen hyperplasia ( J:29510 )

• homozygotes with peritonitis exhibit myeloid hyperplasia in their spleen

abnormal macrophage physiology ( J:29510 )

• in culture, homozygous mutant peritoneal macrophages fail to exhibit LPS induction of PGE2 synthesis

liver/biliary system

abnormal liver morphology ( J:67208 )

• mice that die within the first 48 hrs after birth exhibit macrovesicular and microvesicular lipid deposits in the liver consistent with acute ischemia secondary to heart failure

vision/eye

abnormal induced retina neovascularization ( J:109021 )

• following hypoxia-treatment, the area of retinal nonperfusion is increased compared to in similarly treated wild-type retinas

cellular

patent ductus arteriosus ( J:67208 )

• 33% of mice that die within the first 48 hrs of birth exhibit patent ductus arteriosus

• unlike in wild type mice, treatment with indomethacin does not induce premature closure of the ductus arteriosus and associated neonatal lethality

impaired granulosa cell differentiation ( J:55145 )

• at 8 hrs after hCG treatment, PMSG-primed homozygotes exhibit lack of organized cumulus granulosa cell polarization or expansion

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129/Sv * 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

skeleton

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 96% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

• parathyroid hormone (PTH)-stimulated bone marrow cultures produce fewer TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type cultures

• 1,25-D-stimulated bone marrow cultures exhibit a 60% reduction in pit formation compared with similarly treated wild-type cultures

• spleen cells cultured with RANKL and M-CSF produce 2- to 3-fold fewer osteoclasts than similarly treated wild-type cells

• 1,25-D- or PTH-treated osteoblasts cocultured with wild-type or Ptgs2^tm1Unc homozygous spleen cells exhibit reduced TRAP+ mononuclear cells (osteoclast) formation compared with similarly treated wild-type cells

• however, treatment of cultures with prostaglandin improves osteoclast formation

homeostasis/metabolism

decreased platelet calcium level ( J:124756 )

• serum calcium levels in parathyroid hormone (PTH)-injected mice are lower than in similarly treated wild-type mice

decreased prostaglandin level ( J:124756 )

• 1,25-dihydroxyvitamin D3 (1,25-D)-stimulated bone marrow cultures produce 99% lower prostaglandin levels compared with similarly treated wild-type cultures

• parathyroid hormone (PTH)-stimulated bone marrow cultures produce lower prostaglandin levels compared with similarly treated wild-type cultures

immune system

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 96% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

• parathyroid hormone (PTH)-stimulated bone marrow cultures produce fewer TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type cultures

• 1,25-D-stimulated bone marrow cultures exhibit a 60% reduction in pit formation compared with similarly treated wild-type cultures

• spleen cells cultured with RANKL and M-CSF produce 2- to 3-fold fewer osteoclasts than similarly treated wild-type cells

• however, treatment of cultures with prostaglandin improves osteoclast formation

hematopoietic system

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 96% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

• parathyroid hormone (PTH)-stimulated bone marrow cultures produce fewer TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type cultures

• 1,25-D-stimulated bone marrow cultures exhibit a 60% reduction in pit formation compared with similarly treated wild-type cultures

• spleen cells cultured with RANKL and M-CSF produce 2- to 3-fold fewer osteoclasts than similarly treated wild-type cells

• however, treatment of cultures with prostaglandin improves osteoclast formation

decreased platelet calcium level ( J:124756 )

• serum calcium levels in parathyroid hormone (PTH)-injected mice are lower than in similarly treated wild-type mice

cellular

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 96% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

• parathyroid hormone (PTH)-stimulated bone marrow cultures produce fewer TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type cultures

• 1,25-D-stimulated bone marrow cultures exhibit a 60% reduction in pit formation compared with similarly treated wild-type cultures

• spleen cells cultured with RANKL and M-CSF produce 2- to 3-fold fewer osteoclasts than similarly treated wild-type cells

• however, treatment of cultures with prostaglandin improves osteoclast formation

Allelic Composition	Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	B6.129P2-Ptgs2^tm1Unc

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

decreased prostaglandin level ( J:67211 )

• following occlusion of the middle cerebral artery, mice exhibit an attenuated increase in cortical prostaglandin compared with similarly treated wild-type mice

decreased cerebral infarct size ( J:67211 )

• 96 hours after occlusion of the middle cerebral artery, infarct size is reduced 20% compared to in similarly treated wild-type mice

nervous system

decreased cerebral infarct size ( J:67211 )

• 96 hours after occlusion of the middle cerebral artery, infarct size is reduced 20% compared to in similarly treated wild-type mice

Allelic Composition	Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	D1.129P2(B6J)-Ptgs2^tm1Unc

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

behavior/neurological

increased chemical nociceptive threshold ( J:64383 )

• heterozygous female mutants exhibit fewer writhing responses and decreased nociception in the acetic acid-induced stretch model of algesia

Allelic Composition	Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	D1.129P2-Ptgs2^tm1Unc

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

increased susceptibility to diet-induced obesity ( J:102779 )

• mice fed a high fat and sucrose diet exhibit a 24% greater increase in body weight compared with similarly treated wild-type mice and a 34% increase compared with homozygotes

increased circulating insulin level ( J:102779 )

• in mice fed a high fat and sucrose diet compared to in similarly treated wild-type mice or homozygotes

increased circulating leptin level ( J:102779 )

• leptin serum levels are 336% higher in mice fed a high fat and sucrose diet compared to in similarly treated wild-type mice

increased prostaglandin level ( J:102779 )

• fat pad tissue from mice fed a high fat and sucrose diet exhibit a 2-fold increase in prostaglandin production compared with tissues from similarly treated wild-type mice

adipose tissue

decreased total fat pad weight ( J:102779 )

• mice fed a high fat and sucrose diet exhibit a 134% increase in fat pad weight compared to in similarly treated wild-type mice and 328% increase compared to in similarly treated homozygotes

abnormal adipose tissue physiology ( J:102779 )

• cultured adipose tissue from mice fed a high fat and sucrose diet exhibit increased leptin released compared with adipose tissue from similarly treated wild-type mice or homozygotes

growth/size/body

increased body weight ( J:102779 )

• at 7 to 8 weeks, mice fed breeder chow (10% fat) exhibit increased body weight compared with wild-type mice

• however, after 28 weeks mice exhibit normal body weights when fed breeder chow

increased susceptibility to diet-induced obesity ( J:102779 )

• mice fed a high fat and sucrose diet exhibit a 24% greater increase in body weight compared with similarly treated wild-type mice and a 34% increase compared with homozygotes

Allelic Composition	Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

homeostasis/metabolism

impaired febrile response ( J:54450 )

• LPS-treated mice fail to exhibit an increase in core body temperature unlike similarly treated wild-type mice

cardiovascular system

increased systemic arterial systolic blood pressure ( J:155373 )

• during the inactive day and active night, mice exhibit increased systolic blood pressure compared with wild-type mice

• however, stress induced changes in blood pressure are normal

Allelic Composition	Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	involves: 129/Sv * 129P2/OlaHsd * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

skeleton

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 50% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

homeostasis/metabolism

decreased prostaglandin level ( J:124756 )

• 1,25-dihydroxyvitamin D3 (1,25-D)-stimulated bone marrow cultures produce 62% lower prostaglandin levels compared with similarly treated wild-type cultures

immune system

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 50% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

hematopoietic system

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 50% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

cellular

abnormal osteoclast differentiation ( J:124756 )

• cultured bone marrow treated with 1,25-dihydroxyvitamin D3 (1,25-D) produce 50% less TRAP+ mononuclear cells (osteoclast) than similarly treated wild-type bone marrow

Allelic Composition	Ptgs2^tm1Unc/Ptgs2^tm2.1Hahe
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)
Ptgs2^tm2.1Hahe mutation (1 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to xenobiotic induced morbidity/mortality ( J:158426 )

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice

immune system

increased susceptibility to induced colitis ( J:158426 )

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice

neoplasm

neoplasm ( J:158426 )

N	• mice treated with azoxymethane and dextran sulfate sodium exhibit wild-type colon tumor incidence and histology

digestive/alimentary system

increased susceptibility to induced colitis ( J:158426 )

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice

homeostasis/metabolism

increased susceptibility to xenobiotic induced morbidity/mortality ( J:158426 )

• mice treated with azoxymethane and dextran sulfate sodium exhibit increased mortality compared with similarly treated wild-type mice

Allelic Composition	Ptgs1^tm1Unc/Ptgs1^tm1Unc Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * CD-1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptgs1^tm1Unc mutation (0 available); any Ptgs1 mutation (44 available)
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

neonatal lethality, complete penetrance ( J:64073 )

• mice die within 24 hours of birth with wide patent ductus arterious

cardiovascular system

patent ductus arteriosus ( J:64073 )

cellular

patent ductus arteriosus ( J:64073 )

Allelic Composition	Ptgs1^tm1Unc/Ptgs1^tm1Unc Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

neonatal lethality, incomplete penetrance ( J:67208 )

• more than 50% of mice become cyanotic and die within the first 30 minutes of Caesarian delivery

postnatal lethality, complete penetrance ( J:67208 )

• 100% of mice die within the first 48 hours of birth

cardiovascular system

patent ductus arteriosus ( J:67208 )

• all mice exhibit patent ductus arteriosus

• unlike in wild type mice, treatment with indomethacin does not induce premature closure of the ductus arteriosus and associated neonatal lethality

respiratory system

respiratory distress ( J:67208 )

• in mice that die within the first 30 minutes of delivery

homeostasis/metabolism

cyanosis ( J:67208 )

• more than 50% of mice become cyanotic and die within the first 30 minutes of Caesarian delivery

cellular

patent ductus arteriosus ( J:67208 )

• all mice exhibit patent ductus arteriosus

• unlike in wild type mice, treatment with indomethacin does not induce premature closure of the ductus arteriosus and associated neonatal lethality

Allelic Composition	Ptgs1^tm1Unc/Ptgs1⁺ Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

postnatal lethality, complete penetrance ( J:67208 )

• 79% of mice die within the first 48 hours of birth

cardiovascular system

patent ductus arteriosus ( J:67208 )

• 74% of mice that die within the first 48 hrs of birth exhibit patent ductus arteriosus

cellular

patent ductus arteriosus ( J:67208 )

• 74% of mice that die within the first 48 hrs of birth exhibit patent ductus arteriosus

Allelic Composition	Ptgs1^tm1Unc/Ptgs1⁺ Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

delayed parturition ( J:67208 )

• parturition is delayed

Allelic Composition	Ptgs1^tm1Unc/Ptgs1^tm1Unc Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

reproductive system

delayed parturition ( J:67208 )

• parturition is delayed

Allelic Composition	Apc^Min/Apc⁺ Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6J

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apc^Min mutation (12 available); any Apc mutation (154 available)
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:64401 )

• mice survive 1 year unlike Apc^Min heterozygotes that die after 7 to 8 months

neoplasm

decreased tumor incidence ( J:64401 )

• mice form 84% fewer, smaller intestinal tumors compared with Apc^Min heterozygotes

homeostasis/metabolism

decreased prostaglandin level ( J:64401 )

• intestinal tumor tissue fails to exhibit an increase in prostaglandin levels unlike in Apc^Min heterozygotes

digestive/alimentary system

intestine polyps ( J:64401 )

Allelic Composition	Hr^hr/Hr^hr Ptgs2^tm1Unc/Ptgs2^tm1Unc
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * SKH1

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hr^hr mutation (17 available); any Hr mutation (84 available)
Ptgs2^tm1Unc mutation (0 available); any Ptgs2 mutation (72 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

premature death ( J:121635 )

• mice do not survive beyond several weeks of age

Allelic Composition	Hr^hr/Hr^hr Ptgs2^tm1Unc/Ptgs2⁺
Genetic Background	involves: 129P2/OlaHsd * C57BL/6 * SKH1

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

decreased incidence of tumors by UV induction ( J:121635 )

• after 14 weeks of UV treatment, mice fail to develop tumors unlike similarly treated SKH mice and do not develop tumors until 24 weeks of treatment

• UV-treated mice exhibit a 65% reduction in tumor number and decreased tumor incidence compared with similarly treated wild-type mice

homeostasis/metabolism

decreased prostaglandin level ( J:121635 )

• 50% in the epidermis

cellular

increased cell proliferation ( J:121635 )

• skin from UV-treated mice exhibits 50% less basal cell proliferation than in skin from similarly treated wild-type mice

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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