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Article: MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways
Title | MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways |
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Authors | |
Issue Date | 2022 |
Publisher | Hindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/oximed/ |
Citation | Oxidative Medicine and Cellular Longevity, 2022, v. 2022, p. 2022:3449739 How to Cite? |
Abstract | Acute myocardial infarction is a leading cause of death worldwide, while restoration of blood flow to previously ischemic myocardium may lead to ischemia/reperfusion (I/R) injury. Accumulated evidence shows that microRNAs play important roles in cardiovascular diseases. However, the potential role of microRNA-503 (miR-503) in myocardial I/R injury is little known. Thus, this study is aimed at determining whether and how miR-503 affects myocardial I/R injury in vivo and in vitro. A mouse model of myocardial I/R injury and H9c2 cell model of hypoxia/reoxygenation (H/R) injury were established. The postischemic cardiac miR-503 was downregulated in vivo and in vitro. Mechanistically, PI3K p85 and Bcl-2 are miR-503 targets. The post-ischemic cardiac PI3K p85 protein level was decreased in vivo. Agomir-503 treatment exacerbated H/R-induced injuries manifested as decreased cell viability, increased lactate dehydrogenase activity, and cell apoptosis. Agomir-503 treatment reduced cell viability under normoxia as well and reduced both PI3K p85 and Bcl-2 protein levels under either normoxia or H/R condition. It reduced phosphorylation of Stat3 (p-Stat3-Y705) and Akt (T450) in cells subjected to H/R. In contrast, Antagomir-503 treatment attenuated H/R injury and increased p-Stat3 (Y705) under normoxia and increased p-Akt (T450) under either normoxia or H/R condition. It is concluded that miR-503 exacerbated I/R injury via inactivation of PI3K/Akt and STAT3 pathways and may become a therapeutic target in preventing myocardial I/R injury. |
Persistent Identifier | http://hdl.handle.net/10722/313232 |
ISSN | 2021 Impact Factor: 7.310 2020 SCImago Journal Rankings: 1.494 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | HE, Y | - |
dc.contributor.author | Cai, Y | - |
dc.contributor.author | Sun, T | - |
dc.contributor.author | Zhang, L | - |
dc.contributor.author | Irwin, MG | - |
dc.contributor.author | Xu, A | - |
dc.contributor.author | Xia, Z | - |
dc.date.accessioned | 2022-06-06T05:48:00Z | - |
dc.date.available | 2022-06-06T05:48:00Z | - |
dc.date.issued | 2022 | - |
dc.identifier.citation | Oxidative Medicine and Cellular Longevity, 2022, v. 2022, p. 2022:3449739 | - |
dc.identifier.issn | 1942-0900 | - |
dc.identifier.uri | http://hdl.handle.net/10722/313232 | - |
dc.description.abstract | Acute myocardial infarction is a leading cause of death worldwide, while restoration of blood flow to previously ischemic myocardium may lead to ischemia/reperfusion (I/R) injury. Accumulated evidence shows that microRNAs play important roles in cardiovascular diseases. However, the potential role of microRNA-503 (miR-503) in myocardial I/R injury is little known. Thus, this study is aimed at determining whether and how miR-503 affects myocardial I/R injury in vivo and in vitro. A mouse model of myocardial I/R injury and H9c2 cell model of hypoxia/reoxygenation (H/R) injury were established. The postischemic cardiac miR-503 was downregulated in vivo and in vitro. Mechanistically, PI3K p85 and Bcl-2 are miR-503 targets. The post-ischemic cardiac PI3K p85 protein level was decreased in vivo. Agomir-503 treatment exacerbated H/R-induced injuries manifested as decreased cell viability, increased lactate dehydrogenase activity, and cell apoptosis. Agomir-503 treatment reduced cell viability under normoxia as well and reduced both PI3K p85 and Bcl-2 protein levels under either normoxia or H/R condition. It reduced phosphorylation of Stat3 (p-Stat3-Y705) and Akt (T450) in cells subjected to H/R. In contrast, Antagomir-503 treatment attenuated H/R injury and increased p-Stat3 (Y705) under normoxia and increased p-Akt (T450) under either normoxia or H/R condition. It is concluded that miR-503 exacerbated I/R injury via inactivation of PI3K/Akt and STAT3 pathways and may become a therapeutic target in preventing myocardial I/R injury. | - |
dc.language | eng | - |
dc.publisher | Hindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/oximed/ | - |
dc.relation.ispartof | Oxidative Medicine and Cellular Longevity | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License | - |
dc.title | MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways | - |
dc.type | Article | - |
dc.identifier.email | Irwin, MG: mgirwin@hku.hk | - |
dc.identifier.email | Xu, A: amxu@hkucc.hku.hk | - |
dc.identifier.email | Xia, Z: zyxia@hku.hk | - |
dc.identifier.authority | Irwin, MG=rp00390 | - |
dc.identifier.authority | Xu, A=rp00485 | - |
dc.identifier.authority | Xia, Z=rp00532 | - |
dc.description.nature | published_or_final_version | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1155/2022/3449739 | - |
dc.identifier.pmid | 35620576 | - |
dc.identifier.pmcid | PMC9130001 | - |
dc.identifier.hkuros | 333377 | - |
dc.identifier.volume | 2022 | - |
dc.identifier.spage | 2022:3449739 | - |
dc.identifier.epage | 2022:3449739 | - |
dc.identifier.isi | WOS:000807123100005 | - |
dc.publisher.place | United States | - |