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HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS
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HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS
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HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS
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Journal Article
HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS
2023
Overview
Background
Myocardial ischemia/reperfusion (I/R) contributes to serious myocardial injury and even death. Therefore, prevention and mitigation of myocardial I/R is particularly important. LncRNA HOTAIR has been reported to be implicated in myocardial I/R progression. However, the detailed molecular mechanism of HOTAIR in cardiomyocyte was explored in myocardial I/R.
Methods
Firstly, cell model of myocardial I/R was established through hypoxia/reoxygenation (H/R). Apoptosis and cell cycle were evaluated utilizing flow cytometry. The corresponding test kits were conducted to monitor the levels of LDH, Caspase3 and Caspase9. The gene expression and protein levels were detected by qPCR and western blot, respectively. RNA pull-down and RIP were performed to verify the interaction between FUS and lncRNA HOTAIR.
Results
In AC16 cardiomyocytes treated with H/R, lncRNA HOTAIR and SIRT3 expression were obviously decreased. Overexpression of HOTAIR or SIRT3 could ameliorate H/R-induced cardiomyocyte injury by promoting cell viability, lowering LDH levels, and suppressing cell apoptosis. Further, lncRNA HOTAIR upregulated the expression of SIRT3 via interacting with FUS, thereby promoting the survival of H/R-injured cardiomyocytes.
Conclusion
LncRNA HOTAIR can improve myocardial I/R by affecting cardiomyocyte survival through regulation of SIRT3 by binding to the RNA binding protein FUS.
Highlights
1. Overexpression of HOTAIR or SIRT3 promotes H/R-induced cardiomyocyte survival.
2. LncRNA HOTAIR regulates the expression of SIRT3 by binding to FUS.
3. HOTAIR/FUS/SIRT3 axis facilitates cardiomyocyte survival under H/R treatment.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Coronary Artery Disease - metabolism
/ FUS
/ Heart
/ Humans
/ Hypoxia
/ Ischemia
/ Medicine
/ Myocardial Ischemia - genetics
/ Myocardial ischemia/reperfusion
/ Myocardial Reperfusion Injury - genetics
/ Myocardial Reperfusion Injury - metabolism
/ Myocardial Reperfusion Injury - prevention & control
/ Myocytes, Cardiac - metabolism
/ Plasmids
/ Proteins
/ Reagents
/ RNA, Long Noncoding - genetics
/ RNA, Long Noncoding - metabolism
/ RNA-Binding Protein FUS - genetics
/ RNA-Binding Protein FUS - metabolism
/ SIRT3
