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Conference Paper: MicroRNA-17-3p inhibits excessive post-hypoxic autophagy and attenuates H9C2 cardiomyocytes reoxygenation injury via PTEN-Akt-mTOR signaling
Title | MicroRNA-17-3p inhibits excessive post-hypoxic autophagy and attenuates H9C2 cardiomyocytes reoxygenation injury via PTEN-Akt-mTOR signaling |
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Authors | |
Issue Date | 2018 |
Publisher | Federation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/ |
Citation | Experimental Biology 2018 Meeting, San Diego, CA, 21-25 April 2018 in The FASEB Journal, 2018, v. 32 n. 1, suppl., p. abstract no. lb595 How to Cite? |
Abstract | BackgroundThe microRNA (miR)-17~92 is one of the best-characterized polycistronic miRNA clusters, which encodes six individual miRNAs and contributes to various cellular and biological processes. In particular, miR-17-3p (a passenger miRNA of miR-17) has been shown to indirectly inhibit Phosphatase and tensin homolog (PTEN) and attenuate myocardial ischemia/reperfusion (I/R) injury, but the underneath mechanism is unclear. Inhibition of PTEN can upregulate Akt/mTOR signaling and therefore suppresses the excessive autophagy, which may be a mechanism that underlies myocardial I/R injury. We, thus, hypothesized that miR-17-3p may protect against hypoxia/reoxygenation (H/R) induced cell injury by inhibiting post-hypoxic excessive autophagy in H9C2 cardiomyocytes via PTEN-Akt-mTOR signaling pathway.Methods and resultsIn rat H9C2 cardiomyocytes, H/R (6 hours hypoxia followed by 6 hours reoxygenation) significantly enhanced the expression of miR-17-3p (P <0.05 vs. Control), which was concomitant by increased lactic acid dehydrogenase (LDH) leakage (cell injury marker, P<0.05 vs. Control) and the levels of p62 and the ratio of LC3II/I (autophagy markers, P<0.05 vs. Control), suggesting that miR-17-3p may be involved in the pathogenesis of H/R induced autophagic cell death. To explore the potential role of miR-17-3p in H/R-induced cell injury, H9C2 cells were transfected with the miR-17-3p agomir or its negative control. The overexpression of miR-17-3p can significantly attenuate H/R-induced cell injury (reduced LDH level, P <0.05 vs. H/R) and inhibit H/R-induced excessive autophagy (decreased levels of p62 and LC3II/I, P <0.05 vs. H/R). Given the important role of PTEN-Akt-mTOR signaling in autophagy, the effects of miR-17-3p on the key events in the PTEN-Akt-mTOR signaling cascade during H/R were examined. As anticipated, miR-17-3p overexpression significantly down-regulated PTEN expression and up-regulated the levels of phosphorylated Akt1 (Thr308) and mTOR (P<0.05 vs. H/R), indicating that the miR-17-3p may protect against excessive post-hypoxic autophagic cell death in H9C2 cardiomyocytes via PTEN-Akt-mTOR signaling pathway.ConclusionUpregulating PTEN-Akt-mTOR axis and the subsequent inhibition of excessive autophagy may represent the major mechanism whereby miR-17-3p attenuates H/R injury in H9C2 cardiomyocytes. |
Description | Abstract |
Persistent Identifier | http://hdl.handle.net/10722/263979 |
ISSN | 2023 Impact Factor: 4.4 2023 SCImago Journal Rankings: 1.412 |
DC Field | Value | Language |
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dc.contributor.author | He, Y | - |
dc.contributor.author | Cai, Y | - |
dc.contributor.author | YAN, D | - |
dc.contributor.author | Zhang, D | - |
dc.contributor.author | Chen, C | - |
dc.contributor.author | Irwin, MG | - |
dc.contributor.author | Wang, S | - |
dc.contributor.author | Xia, Z | - |
dc.date.accessioned | 2018-10-22T07:47:34Z | - |
dc.date.available | 2018-10-22T07:47:34Z | - |
dc.date.issued | 2018 | - |
dc.identifier.citation | Experimental Biology 2018 Meeting, San Diego, CA, 21-25 April 2018 in The FASEB Journal, 2018, v. 32 n. 1, suppl., p. abstract no. lb595 | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | http://hdl.handle.net/10722/263979 | - |
dc.description | Abstract | - |
dc.description.abstract | BackgroundThe microRNA (miR)-17~92 is one of the best-characterized polycistronic miRNA clusters, which encodes six individual miRNAs and contributes to various cellular and biological processes. In particular, miR-17-3p (a passenger miRNA of miR-17) has been shown to indirectly inhibit Phosphatase and tensin homolog (PTEN) and attenuate myocardial ischemia/reperfusion (I/R) injury, but the underneath mechanism is unclear. Inhibition of PTEN can upregulate Akt/mTOR signaling and therefore suppresses the excessive autophagy, which may be a mechanism that underlies myocardial I/R injury. We, thus, hypothesized that miR-17-3p may protect against hypoxia/reoxygenation (H/R) induced cell injury by inhibiting post-hypoxic excessive autophagy in H9C2 cardiomyocytes via PTEN-Akt-mTOR signaling pathway.Methods and resultsIn rat H9C2 cardiomyocytes, H/R (6 hours hypoxia followed by 6 hours reoxygenation) significantly enhanced the expression of miR-17-3p (P <0.05 vs. Control), which was concomitant by increased lactic acid dehydrogenase (LDH) leakage (cell injury marker, P<0.05 vs. Control) and the levels of p62 and the ratio of LC3II/I (autophagy markers, P<0.05 vs. Control), suggesting that miR-17-3p may be involved in the pathogenesis of H/R induced autophagic cell death. To explore the potential role of miR-17-3p in H/R-induced cell injury, H9C2 cells were transfected with the miR-17-3p agomir or its negative control. The overexpression of miR-17-3p can significantly attenuate H/R-induced cell injury (reduced LDH level, P <0.05 vs. H/R) and inhibit H/R-induced excessive autophagy (decreased levels of p62 and LC3II/I, P <0.05 vs. H/R). Given the important role of PTEN-Akt-mTOR signaling in autophagy, the effects of miR-17-3p on the key events in the PTEN-Akt-mTOR signaling cascade during H/R were examined. As anticipated, miR-17-3p overexpression significantly down-regulated PTEN expression and up-regulated the levels of phosphorylated Akt1 (Thr308) and mTOR (P<0.05 vs. H/R), indicating that the miR-17-3p may protect against excessive post-hypoxic autophagic cell death in H9C2 cardiomyocytes via PTEN-Akt-mTOR signaling pathway.ConclusionUpregulating PTEN-Akt-mTOR axis and the subsequent inhibition of excessive autophagy may represent the major mechanism whereby miR-17-3p attenuates H/R injury in H9C2 cardiomyocytes. | - |
dc.language | eng | - |
dc.publisher | Federation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/ | - |
dc.relation.ispartof | The FASEB Journal | - |
dc.title | MicroRNA-17-3p inhibits excessive post-hypoxic autophagy and attenuates H9C2 cardiomyocytes reoxygenation injury via PTEN-Akt-mTOR signaling | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Cai, Y: caidavid@hku.hk | - |
dc.identifier.email | Zhang, D: gzdw@hku.hk | - |
dc.identifier.email | Irwin, MG: mgirwin@hku.hk | - |
dc.identifier.email | Xia, Z: zyxia@hkucc.hku.hk | - |
dc.identifier.authority | Irwin, MG=rp00390 | - |
dc.identifier.authority | Xia, Z=rp00532 | - |
dc.identifier.hkuros | 295400 | - |
dc.identifier.volume | 32 | - |
dc.identifier.issue | 1, suppl. | - |
dc.identifier.spage | abstract no. lb595 | - |
dc.identifier.epage | abstract no. lb595 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0892-6638 | - |