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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
MicroRNA-350 induces pathological heart hypertrophy by repressing both p38 and JNK pathways
Yuzhi Ge1, Shujuan Pan, Di Guan
1Translational Medicine Program, the Military General Hospital of Beijing PLA, Beijing, China.
Biochimica Et Biophysica Acta
|September 25, 2012
Summary
MicroRNA-350 (miR-350) induces pathological cardiac hypertrophy and apoptosis by targeting the SAPK pathway in cardiomyocytes. This study reveals miR-350 as a key regulator in rat heart disease.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- MicroRNA Research
Background:
- MicroRNAs (miRNAs) are implicated in cardiac pathophysiology, but miR-350's role in heart disease remains unknown.
- Understanding miR-350's function is crucial for developing novel therapeutic strategies for cardiac hypertrophy and apoptosis.
Purpose of the Study:
- To investigate the role of miR-350 in pathological cardiac hypertrophy and apoptosis.
- To determine if miR-350 induces cardiac hypertrophy by repressing the SAPK pathway in cardiomyocytes.
Main Methods:
- Microarray profiling and quantitative PCR (qPCR) to measure miR-350 expression.
- Western blotting and luciferase assays to identify miR-350 targets.
- Gain-of-function and loss-of-function studies using miR-350 mimics and antagomirs in cardiomyocytes.
Main Results:
- miR-350 was significantly upregulated in rat hearts after transverse aortic constriction.
- miR-350 directly targets and represses mitogen-activated protein kinase (MAPK) 11/14 and MAPK8/9.
- Overexpression of miR-350 induced cardiomyocyte hypertrophy and apoptosis by suppressing p38 and JNK, leading to NFATc3 activation.
Conclusions:
- miR-350 is a critical regulator of pathological cardiac hypertrophy and apoptosis in rats.
- The SAPK pathway (p38/JNK) is a key mediator of miR-350's pro-hypertrophic and pro-apoptotic effects.
- Targeting miR-350 may offer a therapeutic approach for treating cardiac hypertrophy.
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