homeostasis/metabolism
• in mice fed a high-fat diet
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• in mice fed a high-fat diet
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Allele Symbol Allele Name Allele ID |
Mirc32tm1Thbr targeted mutation 1, Thomas Braun MGI:4359903 |
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Summary |
2 genotypes
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• in mice fed a high-fat diet
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• in mice fed a high-fat diet
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♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
Smooth muscle cells from Mirc32tm1Thbr/Mirc32tm1Thbr mice show a shift from a contractile to a synthetic phenotype
• neointimal lesions are observed in 18-month old arteries
• lesions form between the lamina elastica and the endothelial cells
• lesions can grow to large volumes that thin the media without constricting the vessel
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• the contractility of femorial arterial smooth muscle is 39% less than controls after depolarization by potassium
• maximum Ca2+-induced vasoconstriction is blunted by about 30%
• arterial smooth muscle fails to contract in response to angiotensin II stimulation and only respond poorly to alpha1-adrenoceptor agonist phenylephrine
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• thickness of the smooth muscle cell layer in the femoral artery is reduced by about a third
• reduced thickness of the smooth muscle cell layer in femoral artery is due to smaller size of the smooth muscles cells
• the aorta showed a similar though less severe phenotype
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• diastolic blood pressure under anesthesia is reduced by about 30%
• similar results are observed in awake mice
• angiotensin II administration fails to increase blood pressure to the same extent as in controls
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• systolic blood pressure under anesthesia is reduced by about 14%
• similar results are observed in awake mice
• angiotensin II administration fails to increase blood pressure to the same extent as in controls
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• the contractility of femorial arterial smooth muscle is 39% less than controls after depolarization by potassium
• maximum Ca2+-induced vasoconstriction is blunted by about 30%
• arterial smooth muscle fails to contract in response to angiotensin II stimulation and only respond poorly to alpha1-adrenoceptor agonist phenylephrine
|
• neointimal lesions with macrophages and smooth muscle cells are observed in 18-month old arteries
• lesions form between the lamina elastica and the endothelial cells
• lesions can grow to large volumes that thin the media without constricting the vessel
|
• neointimal lesions with macrophages and smooth muscle cells are observed in 18-month old arteries
• lesions form between the lamina elastica and the endothelial cells
• lesions can grow to large volumes that thin the media without constricting the vessel
|
• the contractility of femorial arterial smooth muscle is 39% less than controls after depolarization by potassium
• maximum Ca2+-induced vasoconstriction is blunted by about 30%
• arterial smooth muscle fails to contract in response to angiotensin II stimulation and only respond poorly to alpha1-adrenoceptor agonist phenylephrine
|
• thickness of the smooth muscle cell layer in the femoral artery is reduced by about a third
• reduced thickness of the smooth muscle cell layer in femoral artery is due to smaller size of the smooth muscles cells
• the aorta showed a similar though less severe phenotype
|
• the contractility of femorial arterial smooth muscle is 39% less than controls after depolarization by potassium
• maximum Ca2+-induced vasoconstriction is blunted by about 30%
• arterial smooth muscle fails to contract in response to angiotensin II stimulation and only respond poorly to alpha1-adrenoceptor agonist phenylephrine
|
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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last database update 12/10/2024 MGI 6.24 |
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