OBJECTIVE: Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia-reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. METHODS: miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed. RESULTS: I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice. CONCLUSION: LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression.
LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88.
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作者:Gao Feng, Wang Xiaochen, Fan Tingting, Luo Zhidan, Ma Mengqing, Hu Guangquan, Li Yue, Liang Yi, Lin Xianhe, Xu Banglong
| 期刊: | Molecular Medicine | 影响因子: | 6.400 |
| 时间: | 2022 | 起止号: | 2022 Mar 10; 28(1):33 |
| doi: | 10.1186/s10020-022-00452-1 | ||
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