MicroRNA-210 alleviates oxidative stress-associated cardiomyocyte apoptosis by regulating BNIP3

Diao, Hong-Ying; Liu, Bin; Shi, Yongfeng; Song, Chunli; Guo, Ziyuan; Liu, Ning; Song, Xianjing; Yang, Lu; Lin, Xiaoye; Li, Zhuoran

doi:10.1080/09168451.2017.1343118

Cited by 36 publications

(32 citation statements)

References 41 publications

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“…Bnip3-related mitophagy is also confirmed as one of key mechanism to mediate the role of dual-specificity protein phosphatase1in alleviating cardiac I/R injury [25]. In addition, miR-210 is shown to alleviate oxidative stress-associated cardiomyocyte apoptosis through targeting Bnip3 [26]. In this study, Bnip3 overexpression significantly reversed the impacts of pc-RP4 and miR-939 mimic on hypoxia-disposed damage in H9c2 cells.…”

Section: Discussionsupporting

confidence: 56%

Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/Bnip3/Wnt/β-catenin pathway

Rong

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Section: Discussionsupporting

confidence: 56%

Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/Bnip3/Wnt/β-catenin pathway

Rong

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…4 Meanwhile, other miRNAs, such as miR-210, miR-143, miR-25, miR-1, and miR-133 were identified to participate in the regulation of cardiomyocytes ROS production which lead to oxidative stress-associated apoptosis. [24][25][26][27][28] It could be supposed that lncRNAs-miRNAs-mRNAs interaction would be important regulatory network during diabetic cardiomyopathy pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

RNA‐Seq analysis and functional characterization revealed lncRNA NONRATT007560.2 regulated cardiomyocytes oxidative stress and apoptosis induced by high glucose

Ming

Shan

Liu

et al. 2019

J of Cellular Biochemistry

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Hyperglycemia in diabetic patients would cause cardiomyocytes oxidative stress and apoptosis due to the excessive reactive oxygen species (ROS) accumulation, leading to progressive deterioration of cardiac structure and function. Long noncoding RNAs (lncRNAs) play essential roles on controlling oxidative stress and apoptotic activity. In the present study, RNA sequencing was used to detect the differentially expressed lncRNAs during high glucose‐induced cardiomyocytes oxidative stress and apoptosis. A total of 306/400 lncRNAs were identified as differentially expressed, including 156/198 lncRNAs with increased expression and 150/202 lncRNAs with decreased expression at 24 hours/48 hours after high‐glucose stimulation respectively. Among these dysregulated lncRNAs, 45 lncRNAs were consistently differentially expressed in cardiomyocytes at both two time points after high‐glucose stimulation. Twenty lncRNAs were upregulated and 25 lncRNAs were downregulated at both 24 hours and 48 hours, respectively. The top three upregulated lncRNAs, NONRATT029805.2, NONRATT007560.2, and NONRATT002486.2 were selected for functional studies to determine the role in oxidative stress‐related apoptosis. The results showed that inhibition of non‐ratt007560.2 could abate the formation of ROS and reduce apoptosis, suggesting NONRATT007560.2 might play critical roles in the development of cardiomyopathy. The dysregulated lncRNAs might participate in regulating cardiomyocytes oxidative stress and apoptosis. These findings would be important theoretical and experimental basis for investigation on diabetic cardiomyopathy pathogenesis

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“…it is well known that numerous genes are abnormally expressed in iHd, which are responsible for cardiomyocyte survival and cardiac remodeling following acute and chronic ischemia (32,33). Previous studies have demonstrated that mir-210, as one of several hypoxia-induced mirnas, plays a critical role in cell survival and possesses antiapoptotic properties (34)(35)(36)(37). Supporting evidence suggested that mir-210 expression was ubiquitously and robustly increased in hypoxic cells (34), which is in line with the results of the present study.…”

Section: Discussionmentioning

confidence: 99%

Cardiac shock wave therapy protects cardiomyocytes from hypoxia‑induced injury by modulating miR‑210

et al. 2019

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cardiac shock wave therapy (SWT) has been described as a novel therapeutic strategy that is able to alleviate myocardial ischemic injury. microrna (mirna/mir)-210 plays a cytoprotective role in cardiomyocytes in response to hypoxia by regulating cell apoptosis. The aim of the present study was to investigate whether cardiac SWT could protect cardiomyocytes from hypoxia-induced injury by regulating mir-210 expression. The murine adult cardiomyocyte cell line Hl-1 was incubated for 5 h in hypoxic conditions, followed by reoxygenation for 12 h and treatment with SWT immediately following hypoxia in the present study. The cell viability was determined using an MTS assay. Western blot analyses were performed in order to detect cell signaling changes. reactive oxygen species production was detected using dihydroethidium staining, and malondialdehyde levels were measured using the thiobarbituric acid method. mirna and mrna expression levels were confirmed via reverse transcription-quantitative PCR. Apoptosis was evaluated by means of flow cytometry. Hl-1 cells were then transfected with mir-210 mimics or inhibitors in order to alter mir-210 expression levels, and the effects on Hl-1 cells were determined. Hypoxia led to elevated oxidative stress, enhanced cell apoptosis and upregulated mir-210 expression levels in Hl-1 cells, while SWT could alleviate hypoxia-induced cell injury and further promote mir-210 expression. mir-210 overexpression decreased apoptosis and oxidative stress during hypoxic stress in Hl-1 cells, whereas inhibition of mir-210 increased cell apoptosis and promoted oxidative stress. Furthermore, mir-210 inhibition could reverse the effects of SWT on Hl-1 cells. Finally, the mRNA analysis revealed that SWT significantly attenuated apoptosis-inducing factor mitochondrion-associated 3 and caspase 8 associated protein 2 mrna expression levels in cardiomyocytes exposed to hypoxia, which were two targets of mir-210. SWT could exert cardioprotective effects against hypoxia-induced cardiac injury by modulating mir-210.

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MicroRNA-210 alleviates oxidative stress-associated cardiomyocyte apoptosis by regulating BNIP3

Cited by 36 publications

References 41 publications

Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/Bnip3/Wnt/β-catenin pathway

Upregulation of long noncoding RNA RP4 exacerbates hypoxia injury in cardiomyocytes through regulating miR-939/Bnip3/Wnt/β-catenin pathway

RNA‐Seq analysis and functional characterization revealed lncRNA NONRATT007560.2 regulated cardiomyocytes oxidative stress and apoptosis induced by high glucose

Cardiac shock wave therapy protects cardiomyocytes from hypoxia‑induced injury by modulating miR‑210

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