Phenotypes Associated with This Genotype

Genotype
MGI:4359927

• Allelic Composition: Mirc32^tm1Thbr/Mirc32^tm1Thbr
• Genetic Background: involves: 129/Sv * C57BL/6

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

Smooth muscle cells from Mirc32^tm1Thbr/Mirc32^tm1Thbr mice show a shift from a contractile to a synthetic phenotype

cardiovascular system

abnormal artery morphology ( J:152702 )

• 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

abnormal vascular smooth muscle morphology ( J:152702 )

• 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

vascular smooth muscle hypotrophy ( J:152702 )

• 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

decreased systemic arterial diastolic blood pressure ( J:152702 )

• 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

decreased systemic arterial systolic blood pressure ( J:152702 )

• 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

decreased vasoconstriction ( J:152702 )

• 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

abnormal vascular wound healing ( J:152702 )

• 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

homeostasis/metabolism

abnormal vascular wound healing ( J:152702 )

• 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

muscle

abnormal vascular smooth muscle morphology ( J:152702 )

• 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

vascular smooth muscle hypotrophy ( J:152702 )

• 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

decreased vasoconstriction ( J:152702 )

• 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