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Tcf3‐activated lncRNA Gas5 regulates newborn mouse cardiomyocyte apoptosis in diabetic cardiomyopathy
Author(s) -
Su Dongsheng,
Ju Yansong,
Han Wei,
Yang Yanhua,
Wang Fengyun,
Wang Tong,
Tang Jianmin
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29630
Subject(s) - gas5 , diabetic cardiomyopathy , apoptosis , tunel assay , terminal deoxynucleotidyl transferase , competing endogenous rna , flow cytometry , long non coding rna , microbiology and biotechnology , cancer research , biology , chemistry , cardiomyopathy , rna , heart failure , biochemistry , medicine , gene
Abstract Diabetic cardiomyopathy can cause cardiac dysfunction and eventually lead to heart failure and sudden death. Long noncoding RNA (lncRNA) Gas5 has been reported to play a function in cardiomyocyte. Here we studied the function of Gas5 on newborn mouse cardiomyocyte (NMC) apoptosis to detect its molecular mechanism. High‐glucose treatment was implemented to induce the apoptosis of NMC in this study. And terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, JC‐1 assay, and flow cytometry analysis were conducted to know about the apoptosis of NMC when Gas5 and Tcf3 were silenced. Meanwhile, RNA pull‐down assay and luciferase reporter assay were conducted to verify the binding of RNAs. Finally, rescue assay was implemented to evaluate the influence on apoptosis situation affected by competing endogenous RNA pathways. Tcf3 was found to bind to the Gas5 promoter to activate the expression of Gas5. Meanwhile, Gas5 and Tcf3 were both found to promote the apoptosis of NMC. Also, mmu‐miR‐320‐3p could bind to Gas5 and Tcf3. Moreover, the Gas5/miR‐320‐3p/Tcf3 pathway was found to modulate the apoptosis of NMC. In conclusion, Tcf3‐activated lncRNA Gas5 regulates NMC apoptosis in diabetic cardiomyopathy.