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Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis

Evidence suggests circRBMS1 regulates mRNA to mediate cell apoptosis, inflammation, and oxidative stress in different diseases. MST1 is reported to be the target and activator of apoptosis-related molecules and signaling pathways. Hence, the present study aims to investigate the role of circ-RBMS1/m...

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Autores principales: Liang, Yingping, Jie, Huanhuan, Liu, Qin, Li, Chang, Xiao, Renjie, Xing, Xianliang, Sun, Jing, Yu, Shuchun, Hu, Yanhui, Xu, Guo-hai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9275998/
https://www.ncbi.nlm.nih.gov/pubmed/35611768
http://dx.doi.org/10.1080/21655979.2022.2068896
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author Liang, Yingping
Jie, Huanhuan
Liu, Qin
Li, Chang
Xiao, Renjie
Xing, Xianliang
Sun, Jing
Yu, Shuchun
Hu, Yanhui
Xu, Guo-hai
author_facet Liang, Yingping
Jie, Huanhuan
Liu, Qin
Li, Chang
Xiao, Renjie
Xing, Xianliang
Sun, Jing
Yu, Shuchun
Hu, Yanhui
Xu, Guo-hai
author_sort Liang, Yingping
collection PubMed
description Evidence suggests circRBMS1 regulates mRNA to mediate cell apoptosis, inflammation, and oxidative stress in different diseases. MST1 is reported to be the target and activator of apoptosis-related molecules and signaling pathways. Hence, the present study aims to investigate the role of circ-RBMS1/miR-2355-3p/MST1 in the development of I/R injury. In vitro experiments showed increased circ-RBMS1 and decreased miR-2355-3p in H/R-induced HCMs. CircRBMS1 served as a sponge for miR-2355-3p and miR-2355-3p targeted MST1. Furthermore, knockout of circRBMS1 attenuated cell apoptosis, oxidized stress, and inflammation in H/R-induced HCMs. In vivo experiments indicated circRBMS1 knockdown attenuated cardiac function damage, cell apoptosis, oxidative stress injury and inflammatory response through miR-2355-3p/MST1 axis in mice. In summary, these results demonstrated circRBMS1 played a protective role in myocardial I/R injury though inhibition of miR-2355-3p/MST1 axis. It might provide a new therapeutic target for cardiac I/R injury.
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spelling pubmed-92759982022-07-13 Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis Liang, Yingping Jie, Huanhuan Liu, Qin Li, Chang Xiao, Renjie Xing, Xianliang Sun, Jing Yu, Shuchun Hu, Yanhui Xu, Guo-hai Bioengineered Research Paper Evidence suggests circRBMS1 regulates mRNA to mediate cell apoptosis, inflammation, and oxidative stress in different diseases. MST1 is reported to be the target and activator of apoptosis-related molecules and signaling pathways. Hence, the present study aims to investigate the role of circ-RBMS1/miR-2355-3p/MST1 in the development of I/R injury. In vitro experiments showed increased circ-RBMS1 and decreased miR-2355-3p in H/R-induced HCMs. CircRBMS1 served as a sponge for miR-2355-3p and miR-2355-3p targeted MST1. Furthermore, knockout of circRBMS1 attenuated cell apoptosis, oxidized stress, and inflammation in H/R-induced HCMs. In vivo experiments indicated circRBMS1 knockdown attenuated cardiac function damage, cell apoptosis, oxidative stress injury and inflammatory response through miR-2355-3p/MST1 axis in mice. In summary, these results demonstrated circRBMS1 played a protective role in myocardial I/R injury though inhibition of miR-2355-3p/MST1 axis. It might provide a new therapeutic target for cardiac I/R injury. Taylor & Francis 2022-05-25 /pmc/articles/PMC9275998/ /pubmed/35611768 http://dx.doi.org/10.1080/21655979.2022.2068896 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Liang, Yingping
Jie, Huanhuan
Liu, Qin
Li, Chang
Xiao, Renjie
Xing, Xianliang
Sun, Jing
Yu, Shuchun
Hu, Yanhui
Xu, Guo-hai
Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis
title Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis
title_full Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis
title_fullStr Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis
title_full_unstemmed Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis
title_short Knockout of circRNA single stranded interacting protein 1 (circRBMS1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of miR-2355-3p/Mammalian Sterile20-like kinase 1 (MST1) axis
title_sort knockout of circrna single stranded interacting protein 1 (circrbms1) played a protective role in myocardial ischemia-reperfusion injury though inhibition of mir-2355-3p/mammalian sterile20-like kinase 1 (mst1) axis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9275998/
https://www.ncbi.nlm.nih.gov/pubmed/35611768
http://dx.doi.org/10.1080/21655979.2022.2068896
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