Downregulation of OIP5-AS1 inhibits apoptosis in myocardial ischemia/reperfusion injury via modulating the MiR-145-5p/ROCK1 axis
The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms. In o...
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| Published in | PloS one Vol. 20; no. 5; p. e0324909 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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Public Library of Science
20.05.2025
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| Abstract | The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms.
In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined.
Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions.
Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. |
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| AbstractList | Purpose The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms. Methods In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined. Results Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions. Conclusions Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms. In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined. Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions. Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. Purpose The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms. Methods In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined. Results Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions. Conclusions Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms. In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined. Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions. Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. PurposeThe role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms.MethodsIn order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined.ResultsElevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions.ConclusionsDownregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms.PURPOSEThe role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was conducted with the objective of investigating the function of OIP5-AS1 in myocardial I/R injury and exploring its potential mechanisms.In order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined.METHODSIn order to simulate the conditions of I/R, H9c2 cells were cultured in hypoxic/reoxygenated environments. Induction of I/R in Sprague-Dawley rats was achieved by ligating the left anterior descending coronary artery for 30 minutes followed by 180 minutes of reperfusion. OIP5-AS1 expression levels were assessed, and the degree of apoptosis was evaluated by TUNEL staining. Bioinformatic analysis was conducted to predict the interaction between microRNA-145-5p (miR-145-5p) and OIP5-AS1, and the expression levels of miR-145-5p and ROCK1 were determined.Elevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions.RESULTSElevated levels of OIP5-AS1 were observed in H/R-treated H9c2 cells and in rat I/R models. Elevated OIP5-AS1 expression was associated with an increased incidence of apoptosis. The silencing of OIP5-AS1 in I/R conditions resulted in a significant suppression of cell apoptosis, reduced cleavage of caspase-3, decreased Bax levels, and increased Bcl-2 levels. Bioinformatic analysis predicted binding sites between miR-145-5p and OIP5-AS1. Furthermore, depletion of OIP5-AS1 in I/R conditions resulted in a substantial increase in miR-145-5p expression and a decrease in ROCK1 expression. The suppression of miR-145-5p reversed the effects of OIP5-AS1 depletion in I/R conditions.Downregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis.CONCLUSIONSDownregulation of OIP5-AS1 may prevent apoptosis in myocardial I/R injury by modulating the miR-145-5p/ROCK1 axis. |
| Audience | Academic |
| Author | Xu, Dongling Zhang, Juan Liu, Jing Yang, Jingyan Liu, Xiaobo |
| AuthorAffiliation | 2 Department of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong Province, China Instituto do Cancer do Estado de Sao Paulo / University of Sao Paulo, BRAZIL 1 Department of Pathology, The Second Hospital of Shandong University, Jinan, Shandong Province, China 3 Shandong Blood Center, Jinan, Shandong Province, China |
| AuthorAffiliation_xml | – name: 3 Shandong Blood Center, Jinan, Shandong Province, China – name: Instituto do Cancer do Estado de Sao Paulo / University of Sao Paulo, BRAZIL – name: 1 Department of Pathology, The Second Hospital of Shandong University, Jinan, Shandong Province, China – name: 2 Department of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong Province, China |
| Author_xml | – sequence: 1 givenname: Jingyan surname: Yang fullname: Yang, Jingyan – sequence: 2 givenname: Jing surname: Liu fullname: Liu, Jing – sequence: 3 givenname: Xiaobo surname: Liu fullname: Liu, Xiaobo – sequence: 4 givenname: Dongling surname: Xu fullname: Xu, Dongling – sequence: 5 givenname: Juan orcidid: 0000-0001-6241-7176 surname: Zhang fullname: Zhang, Juan |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/40392837$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1161/CIRCRESAHA.121.318992 10.3389/fphar.2015.00276 10.1038/nrg.2015.10 10.1016/j.molimm.2020.03.015 10.1111/jcmm.14724 10.1007/s10495-022-01760-x 10.1016/j.apsb.2020.03.004 10.1172/JCI62874 10.1371/journal.pgen.1004467 10.1016/j.cell.2018.01.011 10.3389/fcell.2021.773381 10.1016/j.ijcard.2017.05.055 10.1158/1078-0432.CCR-21-0573 10.3892/etm.2021.10228 10.1002/j.1460-2075.1996.tb00574.x 10.3390/cells13100800 10.1016/j.it.2017.08.009 10.1038/nrm2393 10.7554/eLife.12203 10.1016/j.ijcard.2020.01.067 10.1161/CIRCULATIONAHA.118.031373 10.1093/cvr/cvy286 10.1161/CIRCRESAHA.117.311802 10.1155/2021/8889123 10.1016/j.mvr.2023.104565 10.1155/2023/3612814 10.1016/j.hlc.2017.09.011 10.3389/fimmu.2020.599511 10.1016/j.cell.2011.07.014 10.1038/s41556-019-0311-8 10.1038/ncomms4596 10.1056/NEJMra071667 10.3390/cells11071165 |
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| References | J-C Kaski (pone.0324909.ref001) 2018; 138 L Schirone (pone.0324909.ref009) 2022; 11 MJM Silvis (pone.0324909.ref008) 2020; 11 J Wang (pone.0324909.ref006) 2020; 10 W Lone (pone.0324909.ref034) 2021; 27 N Wu (pone.0324909.ref032) 2019; 23 Z Liu (pone.0324909.ref029) 2020; 306 K Wang (pone.0324909.ref027) 2014; 5 LN Maslov (pone.0324909.ref022) 2022; 27 H Xiao (pone.0324909.ref024) 2022; 130 DJ Hausenloy (pone.0324909.ref003) 2013; 123 C Cheng (pone.0324909.ref019) 2021; 22 S Hartmann (pone.0324909.ref031) 2015; 6 Z Zhao (pone.0324909.ref016) 2021; 2021 L Salmena (pone.0324909.ref021) 2011; 146 S-Y Yu (pone.0324909.ref025) 2018; 27 X Niu (pone.0324909.ref018) 2020; 53 F Kopp (pone.0324909.ref011) 2018; 172 DJ Hausenloy (pone.0324909.ref007) 2019; 115 DM Yellon (pone.0324909.ref002) 2007; 357 S Huang (pone.0324909.ref015) 2023; 2023 A Degterev (pone.0324909.ref020) 2008; 9 S-Y Yu (pone.0324909.ref026) 2017; 247 M Laurent (pone.0324909.ref035) 2024; 13 Y Liu (pone.0324909.ref004) 2023; 149 WK Mowel (pone.0324909.ref012) 2018; 39 R-W Yao (pone.0324909.ref010) 2019; 21 K Wang (pone.0324909.ref028) 2014; 10 F Hu (pone.0324909.ref017) 2020; 122 T Matsui (pone.0324909.ref030) 1996; 15 G Heusch (pone.0324909.ref005) 2017; 38 T Sallam (pone.0324909.ref013) 2018; 122 JJ Quinn (pone.0324909.ref014) 2016; 17 Z Xu (pone.0324909.ref023) 2021; 9 S Kümper (pone.0324909.ref033) 2016; 5 |
| References_xml | – volume: 130 issue: 5 year: 2022 ident: pone.0324909.ref024 article-title: CIRKIL exacerbates cardiac ischemia/reperfusion injury by interacting with Ku70 publication-title: Circ Res doi: 10.1161/CIRCRESAHA.121.318992 – volume: 6 start-page: 276 year: 2015 ident: pone.0324909.ref031 article-title: The function of rho-associated kinases ROCK1 and ROCK2 in the pathogenesis of cardiovascular disease publication-title: Front Pharmacol doi: 10.3389/fphar.2015.00276 – volume: 17 start-page: 47 issue: 1 year: 2016 ident: pone.0324909.ref014 article-title: Unique features of long non-coding RNA biogenesis and function publication-title: Nat Rev Genet doi: 10.1038/nrg.2015.10 – volume: 122 start-page: 54 year: 2020 ident: pone.0324909.ref017 article-title: LncRNA 1700020I14Rik/miR-297a/CGRP axis suppresses myocardial cell apoptosis in myocardial ischemia-reperfusion injury publication-title: Mol Immunol doi: 10.1016/j.molimm.2020.03.015 – volume: 23 start-page: 8420 issue: 12 year: 2019 ident: pone.0324909.ref032 article-title: Down-regulation of GAS5 ameliorates myocardial ischaemia/reperfusion injury via the miR-335/ROCK1/AKT/GSK-3β axis publication-title: J Cell Mol Med doi: 10.1111/jcmm.14724 – volume: 27 start-page: 697 year: 2022 ident: pone.0324909.ref022 article-title: The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury publication-title: Apoptosis doi: 10.1007/s10495-022-01760-x – volume: 10 start-page: 1866 issue: 10 year: 2020 ident: pone.0324909.ref006 article-title: Mitochondrial quality control mechanisms as molecular targets in cardiac ischemia-reperfusion injury publication-title: Acta Pharm Sin B doi: 10.1016/j.apsb.2020.03.004 – volume: 123 start-page: 92 issue: 1 year: 2013 ident: pone.0324909.ref003 article-title: Myocardial ischemia-reperfusion injury: a neglected therapeutic target publication-title: J Clin Invest doi: 10.1172/JCI62874 – volume: 10 issue: 7 year: 2014 ident: pone.0324909.ref028 article-title: MDRL lncRNA regulates the processing of miR-484 primary transcript by targeting miR-361 publication-title: PLoS Genet doi: 10.1371/journal.pgen.1004467 – volume: 172 start-page: 393 issue: 3 year: 2018 ident: pone.0324909.ref011 article-title: Functional classification and experimental dissection of long noncoding RNAs publication-title: Cell doi: 10.1016/j.cell.2018.01.011 – volume: 9 start-page: 773381 year: 2021 ident: pone.0324909.ref023 article-title: The novel LncRNA AK035396 drives cardiomyocyte apoptosis through Mterf1 in myocardial ischemia/reperfusion injury publication-title: Front Cell Dev Biol doi: 10.3389/fcell.2021.773381 – volume: 247 start-page: 31 year: 2017 ident: pone.0324909.ref026 article-title: LncRNA UCA1 modulates cardiomyocyte apoptosis by targeting miR-143 in myocardial ischemia-reperfusion injury publication-title: Int J Cardiol doi: 10.1016/j.ijcard.2017.05.055 – volume: 38 start-page: 774 issue: 11 year: 2017 ident: pone.0324909.ref005 article-title: The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge publication-title: Eur Heart J – volume: 27 start-page: 6039 issue: 21 year: 2021 ident: pone.0324909.ref034 article-title: Genome-wide miRNA expression profiling of molecular subgroups of peripheral T-cell lymphoma publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-21-0573 – volume: 22 start-page: 796 issue: 2 year: 2021 ident: pone.0324909.ref019 article-title: MicroRNA-145-5p inhibits hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes by targeting ROCK1 publication-title: Exp Ther Med doi: 10.3892/etm.2021.10228 – volume: 15 start-page: 2208 issue: 9 year: 1996 ident: pone.0324909.ref030 article-title: Rho-associated kinase, a novel serine/threonine kinase, as a putative target for small GTP binding protein Rho publication-title: EMBO J doi: 10.1002/j.1460-2075.1996.tb00574.x – volume: 13 start-page: 800 issue: 10 year: 2024 ident: pone.0324909.ref035 article-title: CRISPR-based gene therapies: from preclinical to clinical treatments publication-title: Cells doi: 10.3390/cells13100800 – volume: 39 start-page: 55 issue: 1 year: 2018 ident: pone.0324909.ref012 article-title: Control of immune cell homeostasis and function by lncRNAs publication-title: Trends Immunol doi: 10.1016/j.it.2017.08.009 – volume: 9 start-page: 378 issue: 5 year: 2008 ident: pone.0324909.ref020 article-title: Expansion and evolution of cell death programmes publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm2393 – volume: 5 year: 2016 ident: pone.0324909.ref033 article-title: Rho-associated kinase (ROCK) function is essential for cell cycle progression, senescence and tumorigenesis publication-title: Elife doi: 10.7554/eLife.12203 – volume: 306 start-page: 9 year: 2020 ident: pone.0324909.ref029 article-title: LncRNA GAS5 exacerbates myocardial ischemia-reperfusion injury through regulating serpina3 by targeting miR-137 publication-title: Int J Cardiol doi: 10.1016/j.ijcard.2020.01.067 – volume: 138 start-page: 1463 issue: 14 year: 2018 ident: pone.0324909.ref001 article-title: Reappraisal of ischemic heart disease publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.118.031373 – volume: 115 start-page: 1143 issue: 7 year: 2019 ident: pone.0324909.ref007 article-title: The coronary circulation in acute myocardial ischaemia/reperfusion injury: a target for cardioprotection publication-title: Cardiovasc Res doi: 10.1093/cvr/cvy286 – volume: 122 start-page: 155 issue: 1 year: 2018 ident: pone.0324909.ref013 article-title: Long noncoding RNA discovery in cardiovascular disease: decoding form to function publication-title: Circ Res doi: 10.1161/CIRCRESAHA.117.311802 – volume: 2021 start-page: 8889123 year: 2021 ident: pone.0324909.ref016 article-title: Long noncoding RNAs in myocardial ischemia-reperfusion injury publication-title: Oxid Med Cell Longev doi: 10.1155/2021/8889123 – volume: 149 start-page: 104565 year: 2023 ident: pone.0324909.ref004 article-title: Myocardial ischemia-reperfusion injury; molecular mechanisms and prevention publication-title: Microvasc Res doi: 10.1016/j.mvr.2023.104565 – volume: 2023 start-page: 3612814 year: 2023 ident: pone.0324909.ref015 article-title: Emodin regulates lncRNA XIST/miR-217 axis to protect myocardial ischemia-reperfusion injury publication-title: Oxid Med Cell Longev doi: 10.1155/2023/3612814 – volume: 27 start-page: 322 issue: 3 year: 2018 ident: pone.0324909.ref025 article-title: Long noncoding RNAs: new players in ischaemia-reperfusion injury publication-title: Heart Lung Circ doi: 10.1016/j.hlc.2017.09.011 – volume: 11 start-page: 599511 year: 2020 ident: pone.0324909.ref008 article-title: Damage-associated molecular patterns in myocardial infarction and heart transplantation: the road to translational success publication-title: Front Immunol doi: 10.3389/fimmu.2020.599511 – volume: 146 start-page: 353 issue: 3 year: 2011 ident: pone.0324909.ref021 article-title: A ceRNA hypothesis: the Rosetta Stone of a hidden RNA language? publication-title: Cell doi: 10.1016/j.cell.2011.07.014 – volume: 21 start-page: 542 issue: 5 year: 2019 ident: pone.0324909.ref010 article-title: Cellular functions of long noncoding RNAs publication-title: Nat Cell Biol doi: 10.1038/s41556-019-0311-8 – volume: 53 issue: 6 year: 2020 ident: pone.0324909.ref018 article-title: lncRNA Oip5-as1 attenuates myocardial ischaemia/reperfusion injury by sponging miR-29a to activate the SIRT1/AMPK/PGC1α pathway publication-title: Cell Prolif – volume: 5 start-page: 3596 year: 2014 ident: pone.0324909.ref027 article-title: CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation publication-title: Nat Commun doi: 10.1038/ncomms4596 – volume: 357 start-page: 1121 issue: 11 year: 2007 ident: pone.0324909.ref002 article-title: Myocardial reperfusion injury publication-title: N Engl J Med doi: 10.1056/NEJMra071667 – volume: 11 start-page: 1165 issue: 7 year: 2022 ident: pone.0324909.ref009 article-title: An overview of the molecular mechanisms associated with myocardial ischemic injury: state of the art and translational perspectives publication-title: Cells doi: 10.3390/cells11071165 |
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| Snippet | The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present study was... Purpose The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present... PurposeThe role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present... Purpose The role of Long noncoding RNA OIP5-AS1 in myocardial ischemia/reperfusion (I/R) injury-induced apoptosis remains to be fully elucidated. The present... |
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| SubjectTerms | Analysis Animal models Animals Antisense RNA Apoptosis Apoptosis - genetics BAX protein Bcl-2 protein Binding sites Biology and Life Sciences Carbon dioxide Cardiomyocytes Cardiomyopathy Care and treatment Caspase-3 Cell Line Complications and side effects Coronary artery Cytotoxicity Depletion Diagnosis Down-Regulation Gene therapy Health aspects Heart diseases Hypoxia Injury prevention Ischemia Kinases Laboratory animals Male Medicine and Health Sciences MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Myocardial ischemia Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Ostomy Patient outcomes Plasmids Proteins Rats Rats, Sprague-Dawley Reperfusion Reperfusion injury Research and Analysis Methods rho-Associated Kinases - genetics rho-Associated Kinases - metabolism RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction |
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| Title | Downregulation of OIP5-AS1 inhibits apoptosis in myocardial ischemia/reperfusion injury via modulating the MiR-145-5p/ROCK1 axis |
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