MiR-495-3p depletion contributes to myocardial ischemia/reperfusion injury in cardiomyocytes by targeting TNC

Song, Wei; Qiu, Naiyan

doi:10.1016/j.reth.2022.08.007

Cited by 4 publications

(3 citation statements)

References 46 publications

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“…To establish a model of MI/RI, according to previous methods, [ 29 ] H9C2 cells were subjected to hypoxia/reoxygenation (H/R). Specifically, H9C2 cells were cultured under 95% N 2 and 5% CO 2 in a humidified chamber for 6 h. Then, the H9C2 cells were exposed to 5% CO 2 and 95% O 2 for another 6 h.…”

Section: Methodsmentioning

confidence: 99%

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

Li,

Wang,

Tan

et al. 2024

J Biochem & Molecular Tox

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Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT‐qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme‐linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit‐8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri‐miR‐199a‐5p m6A modification was detected by Me‐RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R‐induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri‐miR‐199a‐5p m6A methylation to block miR‐199a‐5p maturation and inhibit its expression. TNF receptor‐associated Factor 3 (TRAF3) is a downstream gene of miR‐199a‐5p. Furthermore, in H/R‐induced H9C2 cells, the miR‐199a‐5p inhibitor‐mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression‐mediated promotion of pyroptosis was offset by miR‐199a‐5p upregulation. ALKBH5 silencing inhibited pri‐miR‐199a‐5p expression and enhanced pri‐miR‐199a‐5p m6A modification to promote miR‐199a‐5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression.

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Section: Methodsmentioning

confidence: 99%

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

Li,

Wang,

Tan

et al. 2024

J Biochem & Molecular Tox

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show abstract

“…For instance, miR‐495‐3p is associated with the growth and metastasis of melanoma and colon and liver cancers 15 . It also inhibits the inflammation and differentiation of cardiac cells 16 . However, the effect of miR‐495‐3p on sepsis‐induced vascular endothelial injury remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“… 15 It also inhibits the inflammation and differentiation of cardiac cells. 16 However, the effect of miR‐495‐3p on sepsis‐induced vascular endothelial injury remains unclear.…”

Section: Introductionmentioning

confidence: 99%

lncRNA NEAT1/miR‐495‐3p regulates angiogenesis in burn sepsis through the TGF‐β1 and SMAD signaling pathways

Meng

Hao

Zhang

et al. 2023

Immunity Inflam & Disease

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Introduction:To investigate the role of the long-chain noncoding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) in the process of angiogenesis in human umbilical vein endothelial cells (HUVECs) and illustrate its potential role in burn sepsis (BS) pathogenesis. Methods: HUVECs were treated with BS patient serum or healthy control serum.NEAT1 shRNA, miR-495-3p mimics, and miR-495-3p inhibitor were transfected into HUVECs. NEAT1 and miR-495-3 levels in serum or HUVECs were detected using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 and flow cytometry assays were used to explore the proliferation and apoptosis of HUVECs. The expression of vascular endothelial growth factor (VEGF) in the supernatant was detected using enzyme-linked immunosorbent assay. Tube formation of HUVECs was also analyzed. Western blot analysis was used to analyze signaling pathway proteins.Results: In HUVECs stimulated with BS patient serum, NEAT1 expression was increased, while miR-495-3p expression was decreased. In addition, NEAT1 silencing by specific shRNA inhibited cell proliferation, VEGF production, and tube formation under burn patient serum treatment, which decreased the TGFβ1/SMAD signaling pathway activation. Moreover, miR-495-3p minics inhibited angiogenesis and the activation of signaling pathways induced by NEAT1 shRNA. Furthermore, miR-495-3p inhobitor promoted angiogenesis in HUVECs and activated the TGFβ1/SMAD signaling pathway. In patients with BS, NEAT1 expression was significantly increased and miR-495-3p expression was decreased compared to healthy controls, and NEAT1 and miR-495-3p expression was associated with the clinical features of patients. Conclusions:Our results indicate that lncRNA NEAT1 regulates angiogenesis and activates the TGFβ1/SMAD signaling pathway during the occurrence of BS.

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Ginsenoside Rg3 improves microcystin-induced cardiotoxicity through the miR-128-3p/MDM4 axis

Zhou,

Xia

2023

Drug and Chemical Toxicology

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MiR-495-3p depletion contributes to myocardial ischemia/reperfusion injury in cardiomyocytes by targeting TNC

Cited by 4 publications

References 46 publications

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

lncRNA NEAT1/miR‐495‐3p regulates angiogenesis in burn sepsis through the TGF‐β1 and SMAD signaling pathways

Ginsenoside Rg3 improves microcystin-induced cardiotoxicity through the miR-128-3p/MDM4 axis

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