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Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction

AIMS: Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)‐induced injury of MI. METHODS AND RESULTS: Hypoxia/reoxygenation model of H9C2...

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Autores principales: Wang, Dongmei, Tian, Limei, Wang, Yan, Gao, Xiaoli, Tang, Hanbo, Ge, Junbo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8934946/
https://www.ncbi.nlm.nih.gov/pubmed/35023295
http://dx.doi.org/10.1002/ehf2.13725
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author Wang, Dongmei
Tian, Limei
Wang, Yan
Gao, Xiaoli
Tang, Hanbo
Ge, Junbo
author_facet Wang, Dongmei
Tian, Limei
Wang, Yan
Gao, Xiaoli
Tang, Hanbo
Ge, Junbo
author_sort Wang, Dongmei
collection PubMed
description AIMS: Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)‐induced injury of MI. METHODS AND RESULTS: Hypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real‐time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the stability. Cell counting kit‐8 (CCK‐8), western blot, TUNEL, and flow cytometry assays evaluated cell viability and cell apoptosis. RNA pull‐down, RNA binding protein immunoprecipitation (RIP), and luciferase reporter assays explored the mechanisms underlying MI. All experimental data were presented with mean ± standard deviation (SD) and P < 0.05 indicated statistical significance. Circ_0001206 was low‐expressed in H9C2 cells under H/R treatment. Circ_0001206 was formed by cyclization of CRK like proto‐oncogene, adaptor protein (CRKL). Circ_0001206 overexpression promoted cell viability and inhibited cardiomyocyte apoptosis. It was confirmed that circ_0001206 regulated CRKL expression via acting as a competing endogenous RNA (ceRNA) of microRNA‐665 (miR‐665). CRKL played a protective role in MI. CONCLUSIONS: Circ_0001206 regulates miR‐665/CRKL axis to alleviate H/R‐induced cardiomyocyte injury in MI. Our findings suggest that circ_0001206 might be a potential target for MI treatment.
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spelling pubmed-89349462022-03-24 Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction Wang, Dongmei Tian, Limei Wang, Yan Gao, Xiaoli Tang, Hanbo Ge, Junbo ESC Heart Fail Original Articles AIMS: Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)‐induced injury of MI. METHODS AND RESULTS: Hypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real‐time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the stability. Cell counting kit‐8 (CCK‐8), western blot, TUNEL, and flow cytometry assays evaluated cell viability and cell apoptosis. RNA pull‐down, RNA binding protein immunoprecipitation (RIP), and luciferase reporter assays explored the mechanisms underlying MI. All experimental data were presented with mean ± standard deviation (SD) and P < 0.05 indicated statistical significance. Circ_0001206 was low‐expressed in H9C2 cells under H/R treatment. Circ_0001206 was formed by cyclization of CRK like proto‐oncogene, adaptor protein (CRKL). Circ_0001206 overexpression promoted cell viability and inhibited cardiomyocyte apoptosis. It was confirmed that circ_0001206 regulated CRKL expression via acting as a competing endogenous RNA (ceRNA) of microRNA‐665 (miR‐665). CRKL played a protective role in MI. CONCLUSIONS: Circ_0001206 regulates miR‐665/CRKL axis to alleviate H/R‐induced cardiomyocyte injury in MI. Our findings suggest that circ_0001206 might be a potential target for MI treatment. John Wiley and Sons Inc. 2022-01-13 /pmc/articles/PMC8934946/ /pubmed/35023295 http://dx.doi.org/10.1002/ehf2.13725 Text en © 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
Wang, Dongmei
Tian, Limei
Wang, Yan
Gao, Xiaoli
Tang, Hanbo
Ge, Junbo
Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
title Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
title_full Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
title_fullStr Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
title_full_unstemmed Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
title_short Circ_0001206 regulates miR‐665/CRKL axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
title_sort circ_0001206 regulates mir‐665/crkl axis to alleviate hypoxia/reoxygenation‐induced cardiomyocyte injury in myocardial infarction
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8934946/
https://www.ncbi.nlm.nih.gov/pubmed/35023295
http://dx.doi.org/10.1002/ehf2.13725
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