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A Murine Hypertrophic Cardiomyopathy Model: The DBA/2J Strain
Wenyuan Zhao1, Tieqiang Zhao1, Yuanjian Chen1
1Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee HealthScience Center, Memphis, Tennessee, United States of America.
Plos One
|August 5, 2015
Summary
The DBA/2J mouse strain naturally develops features of hypertrophic cardiomyopathy (HCM), including cardiac hypertrophy and fibrosis, without hypertension. This strain offers a valuable new model for studying HCM genetics and identifying modifier genes.
Area of Science:
- Genetics
- Cardiovascular Biology
- Animal Models
Background:
- Familial hypertrophic cardiomyopathy (HCM) is linked to sarcomere protein gene mutations, but phenotype variability suggests modifier genes play a role.
- Identifying these genetic modifiers is crucial for understanding HCM, yet natural mouse models are scarce.
Purpose of the Study:
- To identify and characterize a natural murine model for hypertrophic cardiomyopathy (HCM).
- To investigate the genetic basis of HCM using the DBA/2J mouse strain.
Main Methods:
- Comparative analysis of Mybpc3 and Myh7 gene sequences between DBA/2J (D2) and C57BL/6J (B6) mouse strains.
- Assessment of cardiac morphology, cardiomyocyte size, and molecular markers of hypertrophy and fibrosis in D2 mice.
- Evaluation of blood pressure and cardiac function in D2 mice.
Main Results:
- The D2 mouse strain exhibits sequence variants in Mybpc3 and Myh7, mirroring human HCM genetics.
- D2 mice show increased heart weight, cardiomyocyte size, and elevated cardiac hypertrophy markers (β-MHC, ANP, BNP, α1-actin).
- Cardiac interstitial fibrosis, with upregulated type I collagen and α-SMA, is present in D2 mice, independent of hypertension or heart failure.
Conclusions:
- The DBA/2J mouse strain represents a novel, natural model for hypertrophic cardiomyopathy (HCM).
- This model exhibits key HCM features, including cardiac hypertrophy and fibrosis, without secondary causes like hypertension.
- The D2 strain's genetic background, particularly its use in BXD recombinant inbred strains, facilitates in-depth genetic analysis of HCM susceptibility and modifier gene discovery.
