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Published on: February 3, 2017
Stem cell antigen 1 protects against cardiac hypertrophy and fibrosis after pressure overload
Heng Zhou1, Zhou-Yan Bian, Jing Zong
1Department of Cardiology, Renmin Hospital of Wuhan University, Jiefang Rd 238, Wuhan 430060, People's Republic of China.
Insights
Stem cell antigen 1 (Sca-1) protects the heart from cardiac hypertrophy and fibrosis. Sca-1 deficiency worsens cardiac dysfunction, while overexpression attenuates it, revealing its protective role in the heart.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Cellular Signaling
Background:
- Stem cell antigen 1 (Sca-1) is a protein implicated in myocardial infarction.
- Sca-1 is upregulated in cardiac hypertrophy models.
- Its precise role in cardiac hypertrophy remains unclear.
Purpose of the Study:
- To investigate the role of Sca-1 in pressure overload-induced cardiac hypertrophy.
- To elucidate the molecular mechanisms underlying Sca-1's function in cardiomyocytes.
Main Methods:
- Cardiac-specific Sca-1 transgenic and knockout mouse models were used.
- Aortic banding was performed to induce cardiac pressure overload.
- Cardiac hypertrophy was assessed via echocardiography, hemodynamics, pathology, and molecular analysis.
Main Results:
- Sca-1 transgenic mice showed attenuated cardiac hypertrophy, fibrosis, and preserved function post-aortic banding.
- Sca-1 knockout mice exhibited exacerbated cardiac hypertrophy, fibrosis, and dysfunction.
- Sca-1 modulated the activation of key signaling pathways including Src, MAPKs, and Akt.
Conclusions:
- Sca-1 plays a protective role against cardiac hypertrophy and fibrosis.
- Sca-1 exerts its protective effects through the regulation of multiple signaling pathways in cardiomyocytes.
- Targeting Sca-1 may offer a therapeutic strategy for cardiac hypertrophy.
Abstract:
Stem cell antigen (Sca) 1, a glycosyl phosphatidylinositol-anchored protein localized to lipid rafts, is upregulated in the heart during myocardial infarction and renovascular hypertension-induced cardiac hypertrophy. It has been suggested that Sca-1 plays an important role in myocardial infarction. To investigate the role of Sca-1 in cardiac hypertrophy, we performed aortic banding in Sca-1 cardiac-specific transgenic mice, Sca-1 knockout mice, and their wild-type littermates. Cardiac hypertrophy was evaluated by echocardiographic, hemodynamic, pathological, and molecular analyses. Sca-1 expression was upregulated and detected in cardiomyocytes after aortic banding surgery in wild-type mice. Sca-1 transgenic mice exhibited significantly attenuated cardiac hypertrophy and fibrosis and preserved cardiac function compared with wild-type mice after 4 weeks of aortic banding. Conversely, Sca-1 knockout dramatically worsened cardiac hypertrophy, fibrosis, and dysfunction after pressure overload. Furthermore, aortic banding-induced activation of Src, mitogen-activated protein kinases, and Akt was blunted by Sca-1 overexpression and enhanced by Sca-1 deficiency. Our results suggest that Sca-1 protects against cardiac hypertrophy and fibrosis via regulation of multiple pathways in cardiomyocytes.
