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Can I read CircRbms1 fosters MST1 mRNA and protein levels to motivate myocardial ischaemia–reperfusion injury via autophagic status on EtoBox?
CircRbms1 fosters MST1 mRNA and protein levels to motivate myocardial ischaemia–reperfusion injury via autophagic status by Qin Liu; Guorong Lai; Yanhui Hu; Fan Yang; Chao Zhang; Dongsheng Le; Fumou Deng; Xianliang Xing; Binquan Tang; Huanhuan Jie; Yingping Liang; Enjun Lei is a Medicine article available to read on EtoBox.
What is CircRbms1 fosters MST1 mRNA and protein levels to motivate myocardial ischaemia–reperfusion injury via autophagic status about?
## Abstract ## Aims Acute myocardial infarction (MI) is a significant contributor to death in individuals diagnosed with coronary heart disease on a worldwide level. The specific mechanism by which circRbms1 contributes to the damage caused by myocardial ischaemia–reperfusion (I/R) is not well understood. The primary aim of this study was to examine the role of circRbms1 and its associated mechanisms in the setting of I/R injury. ## Methods and results An in vivo MI mice model and an in vitro MI cell model was established. The expression levels were detected using quantitative real‐time PCR (qRT‐PCR) and western blot. Cellular proliferation, apoptosis, pyroptosis, and autophagy were detected by immunostaining, immunohistochemistry, western blot, and transmission electron microscopy (TEM). Dual‐luciferase reporter assay, RNA pull‐down assay, and RIP assay were performed to validate the molecular interactions. CircRbms1 was up‐regulated in A/R‐induced HCMs and acted as a sponge for miR‐142‐3p, thereby targeting MST1. CircRbms1 could improve stability of MST1 by recruiting IGF2BP2 (all __P__ < 0.05). CircRbms1 knockout reduced cell pyroptosis, improved autophagy and proliferation leve
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- Author
- Qin Liu; Guorong Lai; Yanhui Hu; Fan Yang; Chao Zhang; Dongsheng Le; Fumou Deng; Xianliang Xing; Binquan Tang; Huanhuan Jie; Yingping Liang; Enjun Lei
- Publisher
- John Wiley and Sons Inc.
- Published
- 2024
- Language
- EN
- Field
- Medicine (Health Sciences)