| Autor: |
Yuan Manli, Jia Huaping, Zhao Bei, Zhang Can, Zuo Xiaowen |
| Jazyk: |
angličtina |
| Rok vydání: |
2023 |
| Předmět: |
|
| Zdroj: |
Open Medicine, Vol 18, Iss 1, Pp 387-407 (2023) |
| Druh dokumentu: |
article |
| ISSN: |
2391-5463 |
| DOI: |
10.1515/med-2023-0681 |
| Popis: |
Long noncoding RNAs (lncRNAs) are known to participate in the pathological process of cardiac hypertrophy. This study aimed to investigate the function of the lncRNA, myosin heavy-chain associated RNA transcript (Mhrt), in cardiac hypertrophy and its possible mechanism of action. Adult mouse cardiomyocytes were treated with angiotensin II (Ang II) and transfected with Mhrt; cardiac hypertrophy was evaluated by estimating atrial natriuretic peptide, brain natriuretic peptide, and beta-myosin heavy-chain levels, and cell surface area by reverse transcription-quantitative polymerase chain reaction, western blotting, and immunofluorescence staining. The interaction between the Mhrt/Wnt family member 7B (WNT7B) and miR-765 was assessed using a luciferase reporter assay. Rescue experiments were performed by analyzing the role of the miR-765/WNT7B pathway underlying the function of Mhrt. The results indicated that Ang II induced hypertrophy of cardiomyocytes; however, overexpression of Mhrt alleviated the Ang II-induced cardiac hypertrophy. Mhrt acted as a sponge for miR-765 to regulate the expression of WNT7B. Rescue experiments revealed that the inhibitory effect of Mhrt on myocardial hypertrophy was abolished by miR-765. Additionally, the knockdown of WNT7B reversed the suppression of myocardial hypertrophy induced by downregulating miR-765. Taken together, Mhrt alleviated cardiac hypertrophy by targeting the miR-765/WNT7B axis. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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