Phenotypes associated with this allele
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation
(6 available);
any
Plat mutation
(61 available)
|
|
|
immune system
|
|
• mice infected with a sublethal dose of mouse-adapted SARS-CoV MA15 show a slight, but not significant, acceleration in recovery of weight loss compared to controls
• mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover
• SARS-CoV MA15 lethally infected mice show a trend toward less hemorrhage in the lungs
• however, SARS-CoV MA15-infected mice show similar viral loads in the lung at 4 and 7 days post infection as wild-type controls
|
|
|
• mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover
|
mortality/aging
|
|
• mice infected with a lethal dose of SARS-CoV MA15 show early mortality compared to wild-type controls, although mice that survive early infection recover
|
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation
(6 available);
any
Plat mutation
(61 available)
|
|
|
behavior/neurological
|
N |
• homozygotes show normal footshock sensitivity thresholds relative to wild-type mice
|
|
|
• homozygotes show no significant differences in the antinociceptive effect of morphine or development of its tolerance relative to wild-type mice
• notably, homozygotes display a significant reduction in morphine-induced hyperlocomotion relative to wild-type
• the defect of morphine-induced hyperlocomotion is reversed by exogenous administration of tPA or plasmin into the nucleus accumbens (Nacc)
|
|
|
• homozygotes display poor active avoidance behavior relative to wild-type mice
|
|
|
• homozygotes display a significant reduction in morphine-induced conditioned place preference
|
|
|
• homozygotes display poor contextual fear conditioning behavior relative to wild-type mice, indicating impaired hippocampal function
|
|
|
• homozygotes display enhanced cue fear conditioning behavior relative to wild-type mice
|
|
|
• relative to wild-type, mutant mice exhibit a 28% reduction in both the rate and extent of learning a complex motor paradigm of irregular peg running, indicating impaired cerebellar motor learning
|
|
|
• homozygotes display no habitation of object exploration relative to wild-type mice
• homozygotes show no reactivity to spatial change (measured as renewed exploration of displaced objects) relative to wild-type mice
|
|
|
• after up to 3 weeks of daily restraint, homozygotes exhibit absence of stress-induced anxiety in the elevated-plus maze; in wild-type, acute stress resuls in a decrease in open arm entries, with 21 days of daily restraint leading to some habituation
(J:81694)
• in response to a low or middle dose of corticotropin-releasing factor (CRF), homozygotes exhibit reduced anxiety (lower number of open arm entries) in the elevated plus-maze, with an increased number of head dips (increased exploration) relative to wild-type
(J:94733)
• in response to a high dose of CRF, homozygotes fail to explore the open arms but display a similar number of closed arms entries relative to wild-type mice, indicating normal locomotor activity
(J:94733)
|
|
|
• in an empty open field, homozygotes show normal horizontal activity but significantly reduced rearing activity relative to wild-type
|
homeostasis/metabolism
immune system
|
|
• in a model of collagen-induced arthritis, severely affected joints from homozygotes display diffuse fibrin(ogen) deposition relative to wild-type
• within arthritic joints, higher fibrin levels appear to correlate with increased disease severity
|
|
|
• in a model of collagen-induced arthritis, arthritic homozygotes exhibit a significant increase in interleukin-1beta levels in the synovium relative to wild-type
• in a model of collagen-induced arthritis, ankle joint washouts from arthritic homozygotes exhibit a significant increase in TNF levels relative to wild-type
|
|
|
• in a model of collagen-induced arthritis, homozygotes develop significant joint inflammation and joint destruction relative to wild-type mice
• severely affected joints from arthritic homozygotes exhibit massive cell infiltration and higher proteoglycan depletion than wild-type mice
|
|
|
• in a model of collagen-induced arthritis, homozygotes develop a significantly more severe arthritis than wild-type mice
• 95% of mutant mice develop arthritis compared with 68% of wild-type mice; no difference in the day of disease onset is observed
• severely affected joints from arthritic homozygotes exhibit higher cartilage damage and bone erosions than wild-type mice
|
muscle
|
N |
• in response to glycerol-induced injury, homozygotes exhibit normal skeletal muscle regeneration after 5 days; regeneration is complete after 9 days
• at 7 days after injury, most injured fibers regenerate into groups of centrally nucleated myotubes, indicating advanced regeneration; only few necrotic fibers are observed
• at 20 days after injury, virtually no signs of muscle injury are detected, except for centrally located myonuclei inside the regenerated fibers
|
skeleton
|
|
• in a model of collagen-induced arthritis, 60% of mutant mice have 3 or 4 affected limbs compared with only 18% of wild-type mice
• in arthritic mutants, 45% of affected individual limbs display severe swelling and/or rigidity compared with only 19% from wild-type
• there are no differences in the degree of swelling (i.e. paw thickness) between limbs from mutant and wild-type mice with the same clinical score
|
|
|
• in a model of collagen-induced arthritis, homozygotes develop significant joint inflammation and joint destruction relative to wild-type mice
• severely affected joints from arthritic homozygotes exhibit massive cell infiltration and higher proteoglycan depletion than wild-type mice
|
|
|
• in a model of collagen-induced arthritis, homozygotes develop a significantly more severe arthritis than wild-type mice
• 95% of mutant mice develop arthritis compared with 68% of wild-type mice; no difference in the day of disease onset is observed
• severely affected joints from arthritic homozygotes exhibit higher cartilage damage and bone erosions than wild-type mice
|
nervous system
|
|
• after restraint, homozygotes show reduced neuronal remodeling in the medial amygdala, with absence of stress-induced ERK1/2 phosphorylation at all time points tested
(J:81694)
• in response to CRF, homozygotes exhibit attenuated expression of Fos (an indicator of neuronal activation) in the central and medial amygdala but show normal Fos responses in paraventricular nuclei
(J:94733)
|
|
|
• in response to tetanic stimulation, hippocampal CA1 slices from mutant mice show a significant reduction in the late phase of LTP relative to wild-type
• notably, a slight but significant reduction of the early phase of hippocampal LTP is also observed
|
|
|
• in response to tetanic stimulation of corticostriatal fibers, homozygotes display absence of LTD in a significant portion of striatal neurons
|
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation
(6 available);
any
Plat mutation
(61 available)
|
|
|
nervous system
|
|
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion
|
|
|
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion
|
homeostasis/metabolism
immune system
|
|
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion
|
hematopoietic system
|
|
• significant decrease in the number of activated glial cells in ischemic tissue after transient middle cerebral artery occlusion
|
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation
(6 available);
any
Plat mutation
(61 available)
|
|
|
mortality/aging
|
N |
• homozygotes display a normal lifespan relative to wild-type mice
|
cardiovascular system
|
|
• in response to laser-induced injury of the Bruch's membrane, homozygotes display almost complete absence of choroidal neovascularization (CNV) at the site of trauma; in contrast, wild-type mice show a robust neovascular reaction
• resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels
|
|
|
• at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
• similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
|
|
|
• in response to pressure overload, wild-type and mutant mice display similar signs of maladaptation (i.e. myolysis, myocardial fibrosis and increased intercapillary distance)
|
|
|
• 11 days after bleomycin treatment, mutant lungs show areas of fibrosis surrounded by areas of extensive intra-alveolar hemorrhage
• hemorrhagic areas contain numerous hemosiderin-laden macrophages, indicating chronic pulmonary hemorrhage
|
|
|
• in a photothrombotic model of middle cerebral artery occlusion (MCAO), delayed heparin administration increases cerebral hemorrhage associated with ischemia in wild-type but NOT in mutant mice
• in this MCAO model, heparin administration induces tPA activity and mRNA expression in microglial cells, and enhances MMP9 expression and proteolytic activation in the ischemic brains of wild-type but NOT of mutant mice
|
|
|
• at 7 weeks after TAB, wild-type and mutant mice exhibit a similar degree of LV dilatation, obvious signs of LV systolic dysfunction, and pump failure
• at 7 weeks after TAB, impaired fractional shortening and abnormal cardiac pump result in respiratory distress due to pulmonary congestion
|
growth/size/body
|
N |
• at 5 weeks of age, homozygotes exhibit a normal body weight relative to wild-type mice
• no macroscopic or histologic abnormalities are observed up to 14 months of age
|
|
|
• at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
• similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
|
hematopoietic system
|
|
• bleomycin-treated homozygotes display a delayed, but significant, increase in macrophage levels reaching wild-type levels at 9 days post-drug treatment
|
immune system
|
N |
• homozygotes exhibit normal matrix degradation and invasion into the peritoneal cavity by thioglycollate-stimulated macrophages
|
|
|
• bleomycin-treated homozygotes display a delayed, but significant, increase in macrophage levels reaching wild-type levels at 9 days post-drug treatment
|
|
|
• after bleomycin treatment, homozygotes exhibit areas of fibrin(ogen) deposits, especially in the vasculature of the lung, where fibrin thrombi are observed
(J:63134)
• after laser-induced injury of the Bruch's membrane, homozygotes show massive accumulation of fibrinogen-fibrin both in the retinal vessels, and in the bottom of the laser-induced trauma
(J:82604)
|
muscle
|
|
• similar to wild-type mice, homozygotes display a ~35% increase in LV/body weight ratio and a ~40% increase in the LV cardiomyocyte size
• at 2 weeks after transverse aortic banding (TAB) i.e. acute pressure overload, homozygotes and wild-type mice exhibit a significant LV hypertrophy which persists for up to 7 weeks
|
|
|
• at 7 weeks after TAB, wild-type and mutant mice exhibit a similar degree of LV dilatation, obvious signs of LV systolic dysfunction, and pump failure
• at 7 weeks after TAB, impaired fractional shortening and abnormal cardiac pump result in respiratory distress due to pulmonary congestion
|
reproductive system
|
N |
• homozygotes display normal litter size and frequency of litters relative to wild-type mice
|
respiratory system
|
|
• 11 days after bleomycin treatment, mutant lungs show areas of fibrosis surrounded by areas of extensive intra-alveolar hemorrhage
• hemorrhagic areas contain numerous hemosiderin-laden macrophages, indicating chronic pulmonary hemorrhage
|
|
|
• bleomycin-treated homozygotes exhibit an enhanced increase in lung hydroxyproline (collagen) content relative to bleomycin-treated wild-type mice
• histological analysis after lung injury indicates extensive interstitial fibrosis in mutant mice relative to wild-type
• notably, homozygotes survive only 11 days post-drug treatment
• 75% of bleomycin-treated homozygotes die as early as 7 days after treatment, as a result of hemorrhage and extensive fibrotic lesions
|
vision/eye
|
|
• in response to laser-induced injury of the Bruch's membrane, homozygotes display almost complete absence of choroidal neovascularization (CNV) at the site of trauma; in contrast, wild-type mice show a robust neovascular reaction
• resistance to CNV is associated with excessive fibrinogen-fibrin deposition at the site of choroidal trauma and in retinal vessels
|
|
|
• at higher doses of NMDA, homozygotes show no differences in retinal damage relative to wild-type mice
• at 12 and 24 h after intravitreal injection of low-dose (30 nmol/mouse) NMDA, homozygotes contain significantly less retinal apoptotic neurons in the ganglion cell layer (GCL) and inner nuclear layer (INL) relative to wild-type; no differences are noted at 72 h after low-dose NMDA injection
|
|
|
• homozygotes are partially resistant to NMDA-induced retinal damage relative to wild-type mice
• in contrast, neither intravitreal kainic acid nor transient ischemia results in significant differences in retinal damage in mutant vs. wild-type mice
|
nervous system
|
|
• in a photothrombotic model of middle cerebral artery occlusion (MCAO), delayed heparin administration increases cerebral hemorrhage associated with ischemia in wild-type but NOT in mutant mice
• in this MCAO model, heparin administration induces tPA activity and mRNA expression in microglial cells, and enhances MMP9 expression and proteolytic activation in the ischemic brains of wild-type but NOT of mutant mice
|
|
|
• homozygotes subjected to focal cerebral ischemia induced by persistent occlusion of the left middle cerebral artery produce an infarct with a size that is significantly smaller than that produced in wild-type mice
|
homeostasis/metabolism
cellular
|
|
• in response to pressure overload, wild-type and mutant mice display similar signs of maladaptation (i.e. myolysis, myocardial fibrosis and increased intercapillary distance)
|
|
|
• at 12 and 24 h after intravitreal injection of low-dose (30 nmol/mouse) NMDA, homozygotes contain significantly less retinal apoptotic neurons in the ganglion cell layer (GCL) and inner nuclear layer (INL) relative to wild-type; no differences are noted at 72 h after low-dose NMDA injection
• at higher doses of NMDA, homozygotes show no differences in retinal damage relative to wild-type mice
|
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation
(6 available);
any
Plat mutation
(61 available)
|
|
|
cardiovascular system
|
|
• aortic vessel explants show almost complete inhibition of capillary sprouting in both collagen lattices and Matrigel
|
|
|
| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Plattm1Mlg mutation
(6 available);
any
Plat mutation
(61 available)
Thbdtm2Rdr mutation
(0 available);
any
Thbd mutation
(23 available)
|
|
|
mortality/aging
|
|
• double homozygotes exhibit a reduced lifespan with 17% dying at ~17 weeks of age
• 9 out of 22 double homozygotes survive until the end of an observation period of 30-40 weeks; only 3 out of 10 double mutants survive until 40-50 weeks
|
integument
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the face
|
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag
|
cellular
|
|
• pre-terminal double mutants display intestinal adhesions and occasionally ischemic tissue necrosis (uterus and intestines), possibly due to thrombosis
|
digestive/alimentary system
|
|
• at 8-12 weeks of age, 37% of double homozygotes display rectal prolapse of a non-infectious origin
• in double mutants, rectal prolapse develops with variable penetrance and onset but appears significantly earlier and at a much higher incidence than in single mutant mice
|
growth/size/body
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the face
|
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag
|
|
|
• at ~17 weeks, 17% of double homozygotes appear runted prior to death
|
|
|
• at 23 weeks, the body weight of double homozygotes is approximately 2/3 that of wild-type mice
|
|
|
• at ~17 weeks, 17% of double homozygotes exhibit cachexia prior to death
|
|
|
• after 3 weeks of age, double homozygotes appear growth retarded relative to wild-type mice
|
hearing/vestibular/ear
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag
|
reproductive system
|
|
• double homozygotes display a significant reduction in fertility possibly because of poor health or large fibrin deposition in the gonads
|
|
|
• double homozygous breeding pairs produce slightly fewer offspring per litter than wild-type breeding pairs
|
respiratory system
|
|
• at ~17 weeks, 17% of double homozygotes exhibit dyspnea prior to death
|
vision/eye
|
|
• at 8-12 weeks of age, 5% of double homozygotes exhibit extensive non-healing ulcerations at the eyelids
|
homeostasis/metabolism
craniofacial
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the face
|
|
|
• at 8-12 weeks of age, 5% of double homozygotes show extensive non-healing ulcerations at the ears around the eartag
|
Analysis Tools