Mitofusin 1 is negatively regulated by MicroRNA 140 in cardiomyocyte apoptosis
Date
2014
Authors
Li, J.
Li, Y.
Jiao, J.
Wang, J.
Li, Y.
Qin, D.
Li, P.
Editors
Advisors
Journal Title
Journal ISSN
Volume Title
Type:
Journal article
Citation
Molecular and Cellular Biology, 2014; 34(10):1788-1799
Statement of Responsibility
Conference Name
Abstract
MicroRNAs (miRNAs) are a class of small noncoding RNAs that mediate post transcriptional gene silencing. Mitochondrial fission participates in the induction of apoptosis. It remains largely unknown whether miRNAs can regulate mitochondrial fission. Reactive oxygen species and doxorubicin could induce mitochondrial fission and apoptosis in cardiomyocytes. Concomitantly, mitofusin 1 (Mfn1) was down regulated, whereas miRNA 140 (miR-140) was up regulated upon apoptotic stimulation. We investigated whether Mfn1 and miR-140 play a functional role in mitochondrial fission and apoptosis. Ectopic expression of Mfn1 attenuated mitochondrial fission and apoptosis. Knockdown of miR-140 inhibited mitochondrial fission. Our results further revealed that knockdown of miR-140 was able to reduce myocardial infarct sizes in an animal model. We observed that miR-140 could suppress the expression of Mfn1, and it exerted its effect on mitochondrial fission and apoptosis through targeting Mfn1. Our data revealed that mitochondrial fission occurs in cardiomyocytes and can be counteracted by Mfn1. However, the function of Mfn1 is negatively regulated by miR-140. Our present work suggests that Mfn1 and miR-140 are integrated into the program of cardiomyocyte apoptosis.
School/Discipline
Dissertation Note
Provenance
Description
Link to a related website: https://mcb.asm.org/content/mcb/34/10/1788.full.pdf, Open Access via Unpaywall
Access Status
Rights
Copyright 2014 American Society for Microbiology