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Phenotypes Associated with This Genotype
Genotype
MGI:6102946
Allelic
Composition
Lrp1tm2Her/Lrp1tm2Her
Tg(Tagln-cre)1Her/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrp1tm2Her mutation (1 available); any Lrp1 mutation (26 available)
Tg(Tagln-cre)1Her mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• increase in heart size in mice older than 36 weeks of age
• heart weight to body weight ratios are increased throughout the age range from 16 to 70 weeks of age

cardiovascular system
• ascending aortas are characterized by increased cell nuclei and fractured elastic laminae and show progressive intra-lamellar thickening, extracellular matrix deposition, and cellular disorganization
• medial layers of the ascending aorta exhibits increased cellular and intracellular accumulation of connective tissue growth factor
• dilation of aortic roots is seen beginning at 16 weeks of age and progresses with age
• dilated ascending aortas in mice older than 36 weeks of age
• coronary arteries within the left ventricle show accumulation of collagen within the tunica media and adventitia
• increase in perivascular fibrosis with outward extension of fibrotic lesions surrounding intramural coronary arteries in 48 week old mice
• extensive and continuous fibrotic lesions tracts extending outward from coronary arteries are sporadically seen in ventricle walls
• increase in myocyte longitudinal area in parenchymal regions of the left ventricle free wall in 48 week old mice
• increase in heart size in mice older than 36 weeks of age
• heart weight to body weight ratios are increased throughout the age range from 16 to 70 weeks of age
• left ventricle enlargement in 48 week old mice
• interstitial fibrosis in intramural coronary arteries of left ventricle free wall and extensive fibrosis in left ventricle papillary muscles
• however, no pericellular fibrosis is seen
• a 38% reduction in fractional shortening and 43% reduction in ejection fraction
• echocardiography shows a reduction in systolic function, with a 38% reduction in fractional shortening, 43% reduction in ejection fraction, and 68% increase in left ventricular diameter in 36 week old mice
• mice show age-dependent increase in incidence of aortic insufficiency, with all mice showing it at 30 weeks of age
• 24 week old mice exhibit a 44% higher pulse pressure than controls
• captopril treatment reduces pulse pressure to levels seen in untreated control mice
• 16% reduction in diastolic pressure in 24 week old mice
• however, systolic blood pressure is normal

muscle
• increase in myocyte longitudinal area in parenchymal regions of the left ventricle free wall in 48 week old mice
• a 38% reduction in fractional shortening and 43% reduction in ejection fraction

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
cardiomyopathy DOID:0050700 J:209752


Contributing Projects:
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
04/13/2021
MGI 6.16
The Jackson Laboratory