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MicroRNA-150 aggravates H2O2-induced cardiac myocyte injury by down-regulating c-myb gene.

Authors: Li, X  Kong, M  Jiang, D  Qian, J  Duan, Q  Dong, A 
Citation: Li X, etal., Acta Biochim Biophys Sin (Shanghai). 2013 Sep;45(9):734-41. doi: 10.1093/abbs/gmt067. Epub 2013 Jul 3.
Pubmed: (View Article at PubMed) PMID:23824072
DOI: Full-text: DOI:10.1093/abbs/gmt067

MicroRNAs (miRNAs) are one class of non-coding RNAs that play an important role in post-transcriptional regulation via the degradation or translational inhibition of their target genes. MicroRNA-150 (miR-150) plays a vital role in regulating the development of B and T lymphocytes. Although the dysregulation of miR-150 was confirmed in human myocardial infarction, little is known regarding the biological functions of miR-150 in response to reactive oxygen species (ROS)-mediated gene regulation in cardiac myocytes. Using quantitative real-time reverse transcription-polymerase chain reaction, we demonstrated that the level of miR-150 was up-regulated in cardiac myocytes after treatment with hydrogen peroxide (H2O2). To identify the potential roles of miR-150 in H2O2-mediated gene regulation, we modulated expression of miR-150 using miR-150 inhibitor and miR-150 mimics. Results showed that silencing expression of miR-150 decreased H2O2-induced cardiac cell death and apoptosis. In lymphocytes, c-myb was a direct target of miR-150. In cardiac myocytes, we found that c-myb was also involved in miR-150-mediated H2O2-induced cardiac cell death. These results suggested that miR-150 participates in H2O2-mediated gene regulation and functional modulation in cardiac myocytes. MiR-150 may play an essential role in heart diseases related to ROS, such as cardiac hypertrophy, heart failure, myocardial infarction, and myocardial ischemia/reperfusion injury.


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CRRD Object Information
CRRD ID: 11532746
Created: 2016-09-06
Species: All species
Last Modified: 2016-09-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.