Related Experiment Video
Updated: May 3, 2026
Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
miR-24 regulates intrinsic apoptosis pathway in mouse cardiomyocytes
1Department of Pathology and Laboratory Medicine; University of North Carolina, Chapel Hill, North Carolina, United States of America ; McAllister Heart Institute, University of North Carolina, Chapel Hill, North Carolina, United States of America.
Abstract:
Numerous cardiac diseases, including myocardial infarction (MI) and chronic heart failure, have been associated with cardiomyocyte apoptosis. Promoting cell survival by inhibiting apoptosis is one of the effective strategies to attenuate cardiac dysfunction caused by cardiomyocyte loss. miR-24 has been shown as an anti-apoptotic microRNA in various animal models. In vivo delivery of miR-24 into a mouse MI model suppressed cardiac cell death, attenuated infarct size, and rescued cardiac dysfunction. However, the molecular pathway by which miR-24 inhibits cardiomyocyte apoptosis is not known. Here we found that miR-24 negatively regulates mouse primary cadiomyocyte cell death through functioning in the intrinsic apoptotic pathways. In ER-mediated intrinsic pathway, miR-24 genetically interacts with the CEBP homologous gene CHOP as knocking down of CHOP partially attenuated the induced apoptosis by miR-24 inhibition. In mitochondria-involved intrinsic pathway, miR-24 inhibits the initiation of apoptosis through suppression of Cytochrome C release and Bax translocation from cytosol to mitochondria. These results provide mechanistic insights into the miR-24 mediated anti-apoptotic effects in murine cardiomyocytes.
Insights
MicroRNA-24 (miR-24) protects heart cells from death by inhibiting apoptosis. This study reveals how miR-24 functions in intrinsic apoptotic pathways to prevent cardiac dysfunction after heart attack.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Death Research
Background:
- Cardiomyocyte apoptosis contributes to cardiac diseases like myocardial infarction (MI) and heart failure.
- Inhibiting apoptosis is a key strategy to preserve heart function and reduce cardiac dysfunction.
- MicroRNA-24 (miR-24) has demonstrated anti-apoptotic properties in preclinical models.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying miR-24's anti-apoptotic effects in cardiomyocytes.
- To investigate miR-24's role in both ER-mediated and mitochondria-involved intrinsic apoptotic pathways.
Main Methods:
- Utilized mouse primary cardiomyocyte cultures.
- Investigated miR-24's interaction with CHOP in the ER-mediated pathway.
- Assessed miR-24's impact on Cytochrome C release and Bax translocation in the mitochondria-involved pathway.
Main Results:
- miR-24 was found to negatively regulate cell death in mouse primary cardiomyocytes via intrinsic apoptotic pathways.
- Knocking down CHOP partially reversed apoptosis induced by miR-24 inhibition, indicating a genetic interaction.
- miR-24 suppressed the initiation of apoptosis by inhibiting Cytochrome C release and Bax translocation to mitochondria.
Conclusions:
- miR-24 exerts anti-apoptotic effects in cardiomyocytes through modulation of intrinsic apoptotic pathways.
- These findings provide crucial mechanistic insights into miR-24's cardioprotective role.
- Understanding miR-24's function may lead to novel therapeutic strategies for heart disease.
More Related Videos
Related Concept Videos
01:31The Intrinsic Apoptotic Pathway
01:17The Extrinsic Apoptotic Pathway
01:22Cellular Injury V: Apoptosis and Autophagy