Cardioprotective effect of miRNA-22 on hypoxia/reoxygenation induced cardiomyocyte injury in neonatal rats

Yang, Jian; Chen, Lihua; Ding, Jiawang; Zhang, Jing; Fan, Zhixing; Yang, Chaojun; Q, Yu; Yang, Jun

doi:10.1016/j.gene.2015.12.037

Cited by 37 publications

(33 citation statements)

References 34 publications

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“…Accumulated studies introduced the miRs and lncRNAs in cardiovascular diseases. Several lncRNAs or miRs are stimulated and functional involved in acute myocardial infarction (eg, ANRIL, KCNQ1OT1, and MALAT1 or miR‐499, and miR‐214) (Vausort et al, ; Janssen et al, ; Xinet al, ), mitochondrial function, and apoptosis of cardiomyocytes (e.g., CHRF or miR‐145, and miR‐22) (Li et al, ; Wang et al, ,; Yang et al, ). Although most lncRNAs have not been defined in myocardial I/R injury, recent studies increasingly focus on the possible contribution of lncRNAs to this progress (Liu et al, , ).…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia‐reperfusion injury

Zhao

Meng

et al. 2016

Cell Biology International

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Long non-coding (lncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also, downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of lncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R). Relative expression of MALAT1, miR-145, and Bnip3 mRNA in cells was determined by quantitative real-time PCR. Cardiomyocyte H/R injury was indicated by lactate dehydrogenase (LDH) release and cell apoptosis. The results showed that fentanyl abrogates expression of responsive gene for H/R and induces downregulation of MALAT1 and Bnip3 and upregulation of miR-145. We found that miR-145/Bnip3 pathway was negatively regulated by MALAT1 in H/R-HL-1 cell with or without fentanyl treatment. Moreover, both MALAT1 overexpression and miR-145 knockdown reverse cardioprotective effects of fentanyl, as indicated by increase in LDH release and cell apoptosis. The reversal effect of MALAT1 for fentanyl is confirmed in cardiac ischemia/reperfusion (I/R) mice. In summary, lncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway.

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Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia‐reperfusion injury

Zhao

Meng

et al. 2016

Cell Biology International

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“…For example, micro-30a-5p might target the 3′UTR of BDNF and down-regulate protein expression of BDNF in humans [15]. And microRNA-22 negatively regulated the expression of CREB binding protein [16]. Muiños-Gimeno M reported that microRNA-16 and microRNA-22 can inhibit the expression of BDNF [17].…”

Section: Introductionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Mediated Perfluorooctane Sulfonate Induced-Neurotoxicity via Epigenetics Regulation in SK-N-SH Cells

Guo

et al. 2017

IJMS

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Perfluorooctane sulfonate (PFOS), a new kind of persistent organic pollutant, is widely distributed in the environment and exists in various organisms, where it is also a neurotoxic compound. However, the potential mechanism of its neurotoxicity is still unclear. To examine the role of epigenetics in the neurotoxicity induced by PFOS, SK-N-SH cells were treated with different concentrations of PFOS or control medium (0.1% DMSO) for 48 h. The mRNA levels of DNA methyltransferases (DNMTs) and Brain-derived neurotrophic factor (BDNF), microRNA-16, microRNA-22, and microRNA-30a-5p were detected by Quantitative PCR (QPCR). Enzyme Linked Immunosorbent Assay (ELISA) was used to measure the protein levels of BDNF, and a western blot was applied to analyze the protein levels of DNMTs. Bisulfite sequencing PCR (BSP) was used to detect the methylation status of the BDNF promoter I and IV. Results of MTT assays indicated that treatment with PFOS could lead to a significant decrease of cell viability, and the treated cells became shrunk. In addition, PFOS exposure decreased the expression of BDNF at mRNA and protein levels, increased the expression of microRNA-16, microRNA-22, microRNA-30a-5p, and decreased the expression of DNMT1 at mRNA and protein levels, but increased the expression of DNMT3b at mRNA and protein levels. Our results also demonstrate that PFOS exposure changes the methylation status of BDNF promoter I and IV. The findings of the present study suggest that methylation regulation of BDNF gene promoter and increases of BDNF-related-microRNA might underlie the mechanisms of PFOS-induced neurotoxicity.

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“…These evidence may indicate the protective effects of miR‐22 in the cardiomyocytes. In addition, Yang et al also revealed miR‐22 might provide a potential cardio‐protective effect on ischemic heart disease through regulating the CBP/AP‐1 pathway to reduce cell apoptosis and inflammatory damage (Yang et al, ). Furthermore, miR‐22 had been found to be elevated in several cancers including colon cancer (Li et al, ) and hepatocellular carcinoma (Zhang et al, ), and it could suppressed the migration and invasion of these cancer cells.…”

Section: Discussionmentioning

confidence: 99%

EA15, MIR22, LINC00472 as diagnostic markers for diabetic kidney disease

Wang

Zhu

Xie

et al. 2018

Journal Cellular Physiology

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This study aimed to investigate the molecular mechanisms of diabetic kidney disease (DKD) and to explore new potential therapeutic strategies and biomarkers for DKD. First we analyzed the differentially expressed changes between patients with DKD and the control group using the chip data in Gene Expression Omnibus (GEO) database. Then the gene chip was subjected to be annotated again, so as to screen long noncoding RNAs (lncRNAs) and study expression differences of these lncRNAs in DKD and controlled samples. At last, the function of the differential lncRNAs was analyzed. A total of 252 lncRNAs were identified, and 14 were differentially expressed. In addition, there were 1,629 differentially expressed messenger RNAs (mRNAs) genes, and proliferation and apoptosis adapter protein 15 (PEA15), MIR22, and long intergenic nonprotein coding RNA 472 ( LINC00472) were significantly differentially expressed in DKD samples. Through functional analysis of the encoding genes coexpressed by the three lncRNAs, we found these genes were mainly enriched in type 1 diabetes and autoimmune thyroid disease pathways, whereas in Gene Ontology (GO) function classification, they were also mainly enriched in the immune response, type I interferon signaling pathways, interferon‐γ mediated signaling pathways, and so forth. To summary, we identified EA15, MIR22, and LINC00472 may serve as the potential diagnostic markers of DKD.

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Cardioprotective effect of miRNA-22 on hypoxia/reoxygenation induced cardiomyocyte injury in neonatal rats

Cited by 37 publications

References 34 publications

Long non‐coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia‐reperfusion injury

Long non‐coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia‐reperfusion injury

Brain-Derived Neurotrophic Factor Mediated Perfluorooctane Sulfonate Induced-Neurotoxicity via Epigenetics Regulation in SK-N-SH Cells

EA15, MIR22, LINC00472 as diagnostic markers for diabetic kidney disease

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