Related Experiment Video
Updated: Feb 15, 2026
Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
Published on: June 29, 2014
MicroRNA-327 regulates cardiac hypertrophy and fibrosis induced by pressure overload
Yue Ji1, Ming Qiu1, Yejiao Shen1
1Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Abstract:
MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin II-induced differentiation into myofibroblasts, as assessed via α-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin II-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin β3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis.
Insights
MicroRNA-327 (miR-327) promotes cardiac fibrosis by activating fibroblast differentiation. Inhibiting miR-327 in mice reduced fibrosis and improved heart function, suggesting miR-327 as a therapeutic target.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Fibrosis Research
Background:
- MicroRNA (miRNA) dysregulation is implicated in cardiac hypertrophy and fibrosis.
- Cardiac fibroblasts play a key role in the development of cardiac fibrosis.
Purpose of the Study:
- To investigate the role of miR-327 in cardiac hypertrophy and fibrosis.
- To explore miR-327 as a potential therapeutic target for cardiac fibrosis.
Main Methods:
- Assessed miR-327 levels in fibroblasts during cardiac hypertrophy.
- Studied the effect of miR-327 induction and knockdown on fibroblast differentiation and gene expression.
- Utilized a mouse model of transverse aortic constriction to evaluate the in vivo effects of miR-327 knockdown.
Main Results:
- miR-327 levels were upregulated in fibroblasts during cardiac hypertrophy and fibrosis.
- Induced miR-327 expression enhanced fibrosis-associated gene expression and myofibroblast differentiation.
- miR-327 knockdown reduced cardiac fibrosis and ventricular dysfunction in a mouse model.
- miR-327 targets integrin β3, diminishing cardiac fibroblast activation.
Conclusions:
- miR-327 plays a significant role in promoting cardiac fibrosis.
- Targeting miR-327 offers a potential therapeutic strategy for reducing cardiac fibrosis and improving cardiac function.
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