Mouse Genome Informatics
hm
    Icam1tm1Bay/Icam1tm1Bay
B6.129S7-Icam1tm1Bay/J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
mortality/aging
• only 2 of 6 mice infected with Plasmodium berghei succumb by day 6 compared with all wild-type C57BL/6 mice
• however, parasitemia is normal
• mutants and wild-type mice treated with streptozotocin to induce diabetes display significantly increased mortality after 12 months of disease compared to untreated controls

vision/eye
• at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~75.7% compared to wild-type mice
• mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type
• in the galactose- and streptozotocin-induced diabetes models, after 11 months, mutants have fewer adherent leukocytes in the retina compared to diabetic controls; number of adherent leukocytes in the retina in 11-month diabetic mutants does not differ from number in non-diabetic controls (J:118466)
• diabetic wild-type mice at 11 months of disease have a 3.1-fold increase in adherent leukocyte number compared with non-diabetic controls (J:118466)
• compared to diabetic wild-type controls, number of endothelial cells in diabetic mutants are higher and comparable to non-diabetic wild-type controls (J:118466)
• 11-month diabetic wild-type mice have 3.8-fold more acellular capillaries compared to non-diabetic controls; in diabetic mutants, this pathology is suppressed by 56% with number of acellular capillaries similar to that in non-diabetic wild-type controls (J:118466)
• at 11 months, numbers of normal appearing pericytes in retinas of diabetic mutants are significantly greater than number in diabetic wild-type controls (J:118466)
• at 22 months, galactosemic mutants show almost less endothelial cell loss (19% vs 25% in galactosemic wild-type mice), no pericyte loss, and less acellular capillary formation (by 55%) than galactosemic wild-type controls compared to euglycemic wild-type mice (J:118466)
• no basement membrane thickening is observed in diabetic and galactosemic mutants compared to that observed in diabetic and galactosemic wild-type controls (J:118466)
• following laser photocoagulation (1,2, and 4 weeks after), significantly less pathologically significant leakage (fewer grade-2B lesions) develops in mutants compared to wild-type (J:119416)
• at weeks 1 and 4, mutants have fewer grade-2B lesions than wild-type mice (J:119416)
• mice have more nonleaky (grade 0) lesions than Icam1-null or wild-type mice at week 4 (J:119416)
• in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months
• in the diabetes models, 11-month diabetic mutants have decreased numbers of injured endothelial cells (<5%) compared to diabetic wild-type controls

cardiovascular system
• at 2 weeks after laser injury, volume of choroidal neovascularization (CNV) is reducedby ~75.7% compared to wild-type mice
• mutants have markedly smaller CNV membranes 2 weeks after injury compared to wild-type
• in diabetes models, mutants exhibit decreased retinal-blood barrier breakdown compared to diabetic controls at 11 months

immune system
N
• leukocytes exhibit normal adhesion in the brain of un-infected and Plasmodium berghei-infected mice (J:193592)
• only 2 of 6 mice infected with Plasmodium berghei succumb by day 6 compared with all wild-type C57BL/6 mice
• however, parasitemia is normal

homeostasis/metabolism
• blood glucose levels are significantly increased in mutants and controls with streptozotocin treatment or high galactose diet

Mouse Models of Human Disease
OMIM IDRef(s)
Malaria, Susceptibility to 611162 J:193592