MicroRNA-210 aggravates hypoxia-induced injury in cardiomyocyte H9c2 cells by targeting CXCR4

Feng, Min; Li, Zongqing; Wang, Dong; Wang, Fang; Wang, Chenyan; Wang, Chunfang; Ding, Faming

doi:10.1016/j.biopha.2018.03.151

Cited by 16 publications

(10 citation statements)

References 29 publications

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“…Other studies lend support to the notion that miR-210 diminishes cardiomyocyte apoptosis induced by oxidative stress [51]. A very recent study reported that the expression of miR-210 is dramatically increased in hypoxic H9c2 cells [52]. Yet this study, in an apparently paradoxical result, reports that when miR-210 is suppressed, hypoxia-induced cardiomyocyte injury was favorably mitigated [52] (Table 1).…”

Section: Micrornas (Mirnas)supporting

confidence: 52%

“…A very recent study reported that the expression of miR-210 is dramatically increased in hypoxic H9c2 cells [52]. Yet this study, in an apparently paradoxical result, reports that when miR-210 is suppressed, hypoxia-induced cardiomyocyte injury was favorably mitigated [52] (Table 1). Regulation of miR-210 expression in response to insulin in the context of I/R injury has also been investigated.…”

Section: Micrornas (Mirnas)mentioning

confidence: 89%

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MicroRNAs as Potential Pharmaco-Targets in Ischemia-Reperfusion Injury Compounded by Diabetes

Dehaini

Awada

El‐Yazbi

et al. 2019

Cells

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Background: Ischemia-Reperfusion (I/R) injury is the tissue damage that results from re-oxygenation of ischemic tissues. There are many players that contribute to I/R injury. One of these factors is the family of microRNAs (miRNAs), which are currently being heavily studied. This review aims to critically summarize the latest papers that attributed roles of certain miRNAs in I/R injury, particularly in diabetic conditions and dissect their potential as novel pharmacologic targets in the treatment and management of diabetes. Methods: PubMed was searched for publications containing microRNA and I/R, in the absence or presence of diabetes. All papers that provided sufficient evidence linking miRNA with I/R, especially in the context of diabetes, were selected. Several miRNAs are found to be either pro-apoptotic, as in the case of miR-34a, miR-144, miR-155, and miR-200, or anti-apoptotic, as in the case of miR-210, miR-21, and miR-146a. Here, we further dissect the evidence that shows diverse cell-context dependent effects of these miRNAs, particularly in cardiomyocytes, endothelial, or leukocytes. We also provide insight into cases where the possibility of having two miRNAs working together to intensify a given response is noted. Conclusions: This review arrives at the conclusion that the utilization of miRNAs as translational agents or pharmaco-targets in treating I/R injury in diabetic patients is promising and becoming increasingly clearer.

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Section: Micrornas (Mirnas)supporting

confidence: 52%

Section: Micrornas (Mirnas)mentioning

confidence: 89%

MicroRNAs as Potential Pharmaco-Targets in Ischemia-Reperfusion Injury Compounded by Diabetes

Dehaini

Awada

El‐Yazbi

et al. 2019

Cells

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“…31 miR-210 modulates proliferation, survival and anti-apoptosis of cardiomyocytes in response to hypoxia stimulation. 31,33 Consistent with previous results, 30,31,33 our findings suggested that both up-regulation of miR-31 and reduction of miR-210 were observed in hypoxia-treated H9c2 cardiomyocytes. Interestingly, leonurine could reverse the hypoxia-induced up-regulation of miR-31 and the reduction of miR-210 in cardiomyocytes.…”

Section: Discussionsupporting

confidence: 91%

Leonurine Alleviates Hypoxia-Induced Myocardial Damage by Regulating miRNAs

Liu

Wang

Luo

et al. 2021

Natural Product Communications

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Objective miRNAs as pharmaco-targets have been investigated in multifarious diseases. Our study aimed to determine whether leonurine was a potential cardioprotective agent by targeting miRNAs in hypoxia-stimulated mice and H9c2 cardiomyocytes. Methods Cell proliferation and apoptosis were examined by CCK-8 and TUNEL assay in hypoxia-stimulated rat H9c2 cardiomyocytes. miRNAs expression levels in cardiomyocytes in response to hypoxia stimulation were detected by RT-qPCR. Mice with myocardial injury were induced by chronic intermittent hypoxia stimulation. Results Leonurine alleviated hypoxia-induced cardiac hypertrophy in mice. Moreover, up-regulation of miR-31 and down-regulation of miR-210 in hypoxia-stimulated mice were reversed by leonurine administration. Leonurine exhibited cardioprotective activity in an vitro cell model of hypoxia-stimulated rat H9c2 cardiomyocytes, reflecting that the compound improved hypoxia-induced growth inhibition and apoptosis of cardiomyocytes. TUNEL assay revealed that transfection of miR-31 inhibitors or miR-210 mimics abrogated hypoxia-induced cardiomyocyte apoptosis. In contrast to that, miR-31 mimics or miR-210 inhibitors counteracted the anti-apoptotic effect of leonurine on hypoxia-treated rat H9c2 cardiomyocytes. Conclusion Our findings suggest that miR-31 and miR-210 as the upstream regulators of leonurine are involved in hypoxia-induced cardiomyocyte apoptosis. Leonurine can target miRNAs to protect against hypoxia-induced myocardial damage. miRNAs as potential drug targets may provide prospective therapeutic strategies for the treatment of myocardial damage.

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“…23) Feng, et al found that overexpressed miR-210 alleviates the hypoxia-induced injury to H9C2 cells by overexpressing miR-210 or silencing miR-210 in H9C2 cells, whereas silencing miR-210 produces the opposite results. 24) To further investigate the protective effect of miR-448-5p on myocardial cells induced by hypoxia injury, miR-448-5p mimic and inhibitor were transfected into the hypoxia model, and the results showed that the cell viability of hypoxia model was inhibited; moreover, its apoptosis was significantly promoted when miR-448-5p was overexpressed, and inhibiting miR-448-5p promoted the viability and reduced the apoptosis of the hypoxia model.…”

Section: Discussionmentioning

confidence: 99%

MiR-448-5p/VEGFA Axis Protects Cardiomyocytes from Hypoxia Through Regulating the FAS/FAS-L Signaling Pathway

et al. 2021

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Bioinformatics analysis showed that miR-448-5p expression in the myocardial tissue of rats with myocardial infarction significantly increased, suggesting that it may participate in myocardial cell apoptosis in myocardial infarction. This study aimed to explore the protective effects of miR-448-5p on hypoxic myocardial cells.H9C2 cells were cultured and subjected to anoxia for 2, 4, and 8 hours to establish a hypoxia model. MiR-448-5p mimic and inhibitor were transfected into the cells; then, a dual-luciferase experiment was conducted to verify the targeting relationship between miR-448-5p and VEGFA. Cell viability and apoptosis was detected by cell counting kit-8 and flow cytometry, respectively. The expressions of apoptosis-related proteins, miR-448-5p, FAS, and FAS-L were measured using western blotting and quantitative reverse transcription-polymerase chain reaction (qRT-PCR).Hypoxia-reduced H9C2 cell viability and promoted apoptosis. MiR-448-5p expression was increased after H9C2 cell hypoxia. MiR-448-5p mimic significantly inhibited the viability and promoted the apoptosis of hypoxia-induced model cells. Hypoxia promoted the expression of apoptosis-related protein B-cell lymphoma-2 (Bcl-2) and inhibited the expressions of Bcl-2-associated x protein (Bax), cleaved caspase-3, and caspase-3, whereas the effect of inhibitor on hypoxia-reduced H9C2 cell and apoptotic protein expression were opposite to miR-448-5p mimic. MiR-448-5p targeted VEGFA and regulated its expression. Silenced VEGFA expression significantly inhibited inhibitor effect on increasing cell viability and promoted apoptosis. In addition, miR-448-5p mimic inhibited the effect of hypoxia on promoting the expressions of FAS and FAS-L of H9C2 cells. Inhibitors had the opposite effect on cell hypoxia model.The miR-448-5p/VEGFA axis could protect cardiomyocytes from hypoxia through inhibiting the FAS/FAS-L signaling pathway.

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MicroRNA-210 aggravates hypoxia-induced injury in cardiomyocyte H9c2 cells by targeting CXCR4

Cited by 16 publications

References 29 publications

MicroRNAs as Potential Pharmaco-Targets in Ischemia-Reperfusion Injury Compounded by Diabetes

MicroRNAs as Potential Pharmaco-Targets in Ischemia-Reperfusion Injury Compounded by Diabetes

Leonurine Alleviates Hypoxia-Induced Myocardial Damage by Regulating miRNAs

MiR-448-5p/VEGFA Axis Protects Cardiomyocytes from Hypoxia Through Regulating the FAS/FAS-L Signaling Pathway

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