MicroRNA-29a-3p attenuates ET-1-induced hypertrophic responses in H9c2 cardiomyocytes
| Autor: | Tie-Feng Song, Jian Zhang, Hui-Qin Gong, Li-Nan Zhang, Nan Wang, Tong-Cun Zhang, Dongsun Cao, Zhi-Xia Guo, Hongpeng He, Man Li, Rui Zhang |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Cardiac fibrosis Down-Regulation Cardiomegaly Nerve Tissue Proteins Biology Cell Line 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Fibrosis microRNA Genetics medicine Animals Myocytes Cardiac RNA Messenger Transcription factor 3' Untranslated Regions Heart Failure Endothelin-1 NFATC Transcription Factors General Medicine medicine.disease Endothelin 1 Rats MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis Heart failure Cancer research |
| Zdroj: | Gene. 585(1) |
| ISSN: | 1879-0038 |
| Popis: | Transcription factor nuclear factor of activated T cells c4 (NFATc4) is the best-characterized target for the development of cardiac hypertrophy. Aberrant microRNA-29 (miR-29) expression is involved in the development of cardiac fibrosis and congestive heart failure. However, whether miR-29 regulates hypertrophic processes is still not clear. In this study, we investigated the potential functions of miR-29a-3p in endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy. We showed that miR-29a-3p was down-regulated in ET-1-treated H9c2 cardiomyocytes. Overexpression of miR-29a-3p significantly reduced ET-1-induced hypertrophic responses in H9c2 cardiomyocytes, which was accompanied by a decrease in NFATc4 expression. miR-29a-3p targeted directly to the 3'-UTR of NFATc4 mRNA and silenced NFATc4 expression. Our results indicate that miR-29a-3p inhibits ET-1-induced cardiomyocyte hypertrophy via inhibiting NFATc4 expression. |
| Databáze: | OpenAIRE |
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