CircRNA-32011 regulates apoptosis induced by arsenic trioxide in cardiac myocytes
- Author:
Wen-Jun MA
1
;
Lin CHANG
1
;
Ji-Chen WU
1
;
Jia-Qi LIU
1
;
Hui FU
1
;
Ying WANG
1
;
Ai-Jing SHANG
2
;
Wen-Zheng CHENG
2
;
Xiao-Xiang GUAN
2
;
Hong ZHANG
2
;
Yuan JIANG
2
;
Chao-Qian XU
2
Author Information
- Publication Type:Journal Article
- Keywords: apoptosis; arsenic trioxide; Bcl-2/Bax; cardio- toxicity; cardiomyocy tes; circRNA-32011
- From: Chinese Pharmacological Bulletin 2022;38(10):1498-1504
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the effect of circRNA- 32011 on myocardial apoptosis induced by arsenic triox- ide (ATO).Methods Primary cardioniyocytes of suckling neonate mouse were treated with ATO ( final concentration 10 (xniol • L_1 ) for 24 h.Then cell via¬bility was measured by M IT assay.The mKNA expres¬sion levels of Bel-2/ Bax and circRNA-3201 I were de¬tected by KT-PCK.Bcl-2/Bax protein expression lev¬els were detected by Western blot.Overexpression and knock down circHNA-32011 respectively by plasmid and siHNA were used to verify its function in ATO-in- duced cardiomyocyte apoptosis.Results Myocardial cell viability decreased, Bel-2 expression significantly decreased while Bax expression increased in ATO group compared with the control group.CircKNA- 32011 was down-regulated in ATO ineuhated cardio¬niyocytes.Ovcrex press ion of circRNA-32011 in ATO- incubated cardioniyocytes increased myocardial cell vi¬ability and Bel-2 expression and decreased the expres¬sion of Bax.Knockdown of circRNA-32011 could fur¬ther reduce cardiomyoevte activity and Bel-2 expression and increase the experssion of Bax induced by ATO.Conclusions CircRNA-32011 protects cardiac myo¬cytes from apoptosis induced by arsenic trioxide, which may provide a new potential therapeutic strategy for ATO-induced myocardial injury.
