Phenotypes Associated with This Genotype

Genotype
MGI:3525858

• Allelic Composition: Mapk14^tm1.2Otsu/Mapk14^tm1.2Otsu; Tg(Myh6-cre)2182Mds/0
• Genetic Background: involves: C57BL/6J

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

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:95116 )

• 30% of mutants died one week after TAC induced pressure overload compared to 8% in controls

cardiovascular system

enlarged heart ( J:95116 )

• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation

increased heart weight ( J:95116 )

• heart weight, left ventricle weight, and average ratio of left ventricle weight to tibial length or body weight were significantly greater than in controls after TAC induced pressure overload, however no difference in cardiomyocyte cell area was observed

cardiac fibrosis ( J:95116 )

• observed intermuscular and perivascular fibrosis in mutants compared to only slight perivascular fibrosis in controls after TAC induced pressure overload

decreased cardiac muscle contractility ( J:95116 )

• mice exhibit normal cardiac function and structure under baseline conditions, however cardiac contractility was significantly reduced after thoracic transverse aortic constriction (TAC) induced pressure overload and chronic adrenergic stimulation

decreased heart left ventricle muscle contractility ( J:95116 )

• increased left ventricle end-diastolic and end-systolic diameters compared to controls after TAC induced pressure overload

increased response of heart to induced stress ( J:95116 )

• after TAC induced pressure overload, exhibit greater increases in mortality, heart size and weight, cardiac fibrosis, and cardiomyocyte apoptosis and decreased cardiac contractility compared to controls

muscle

decreased cardiac muscle contractility ( J:95116 )

• mice exhibit normal cardiac function and structure under baseline conditions, however cardiac contractility was significantly reduced after thoracic transverse aortic constriction (TAC) induced pressure overload and chronic adrenergic stimulation

decreased heart left ventricle muscle contractility ( J:95116 )

• increased left ventricle end-diastolic and end-systolic diameters compared to controls after TAC induced pressure overload

increased cardiomyocyte apoptosis ( J:95116 )

• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation

homeostasis/metabolism

increased response of heart to induced stress ( J:95116 )

• after TAC induced pressure overload, exhibit greater increases in mortality, heart size and weight, cardiac fibrosis, and cardiomyocyte apoptosis and decreased cardiac contractility compared to controls

cellular

increased cardiomyocyte apoptosis ( J:95116 )

• the number of apoptotic cardiac myocytes was 3.7 times that in controls after TAC induced pressure overload and was also increased in response to chronic adrenergic stimulation

growth/size/body

enlarged heart ( J:95116 )

• heart was larger than in controls after TAC induced pressure overload or adrenergic stimulation

increased heart weight ( J:95116 )

• heart weight, left ventricle weight, and average ratio of left ventricle weight to tibial length or body weight were significantly greater than in controls after TAC induced pressure overload, however no difference in cardiomyocyte cell area was observed