Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmox1tm1Mlee mutation
(0 available);
any
Hmox1 mutation
(33 available)
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cardiovascular system
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• in response to vascular injury in femoral arteries, homozygotes display hyperplastic arteries relative to wild-type mice (intima:media area ratios of arterial lesions, 2.0 +/- 0.3 versus 1.1 +/- 0.2, respectively)
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• mutant VSMCs exhibit enhanced DNA synthesis and growth relative to wild-type VSMCs, as a result of facilitated G1/S entry
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• in response to vascular injury, homozygotes exhibit a ~5-fold increase in VSMC proliferation in femoral arteries relative to wild-type mice
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cellular
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• in response to vascular injury, homozygotes exhibit a ~5-fold increase in VSMC proliferation in femoral arteries relative to wild-type mice
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muscle
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• mutant VSMCs exhibit enhanced DNA synthesis and growth relative to wild-type VSMCs, as a result of facilitated G1/S entry
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• in response to vascular injury, homozygotes exhibit a ~5-fold increase in VSMC proliferation in femoral arteries relative to wild-type mice
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hmox1tm1Mlee mutation
(0 available);
any
Hmox1 mutation
(33 available)
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mortality/aging
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• all mice infected with Plasmodium chabaudi chabaudi die unlike control mice without an increase in parasitemia
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• only ~20% of newborn homozygotes are obtained from heterozygote breedings, suggesting partial perinatal lethality
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• at 3 weeks, only about 7% of homozygotes are obtained from heterozygote matings; surviving homozygotes appear grossly normal
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cardiovascular system
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display mononuclear inflammatory cell infiltration and extensive cardiomyocyte degeneration and death with focal calcification, characteristic of infarcts which are 1-2 weeks old
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes exhibit a greater increase in right ventricular weight relative to wild-type mice
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• in response to chronic hypoxia (10% oxygen, 5-7 weeks), homozygotes show comparable increases in hematocrit values, pulmonary hypertension (right ventricular systolic pressure) and pulmonary vascular remodeling (peripheral muscularized vessels) relative to wild-type mice
• however, in response to chronic hypoxia (10% oxygen, 5 weeks), homozygotes exhibit increased right ventricular dilation relative to wild-type mice, with severe dilation noted at 7 weeks
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes exhibit increased perivascular fibrosis, with earlier collagen deposition and scar formation surrounding infarcted sites relative to wild-type mice
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display increased cardiomyocyte apoptosis, as shown by increased TUNEL-positive cells in infarcted areas
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• in response to chronic hypoxia (10% oxygen, 7 weeks), 4 of 6 homozygotes exhibit evidence of right ventricular infarcts which are less than 2 weeks old
• however, no left ventricular infarcts or coronary occlusion are observed
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homeostasis/metabolism
cellular
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display mononuclear inflammatory cell infiltration and extensive cardiomyocyte degeneration and death with focal calcification, characteristic of infarcts which are 1-2 weeks old
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display increased cardiomyocyte apoptosis, as shown by increased TUNEL-positive cells in infarcted areas
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes show extensive lipid peroxidation and oxidative damage in the zone of right ventricular infarctions
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muscle
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display mononuclear inflammatory cell infiltration and extensive cardiomyocyte degeneration and death with focal calcification, characteristic of infarcts which are 1-2 weeks old
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• in response to chronic hypoxia (10% oxygen, 7 weeks), homozygotes display increased cardiomyocyte apoptosis, as shown by increased TUNEL-positive cells in infarcted areas
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immune system
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• mice infected with Plasmodium chabaudi chabaudi (PCC) exhibit increased mortality and hepatic failure with a 4-fold increase in alanine aminotransferase plasma concentration and accumulation of thiobarbituric acid reactive substances compared with control mice
• mice infected with Plasmidium berhei ANKA exhibit increased cerebral malaria as indicated by brain edema compared with control mice
• however, mice infected with PCC exhibit normal parasitemia and do not develop cerebral malaria or kidney failure
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• all mice infected with Plasmodium chabaudi chabaudi die unlike control mice without an increase in parasitemia
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liver/biliary system
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• in mice infected with Plasmodium chabaudi chabaudi
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nervous system
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• in mice infected with Plasmidium berhei ANKA
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Analysis Tools