Author:
Li Jun,Wang Hao,Chen Li,Zhong Jialin,Wang Junsheng,Xiao Jun
Abstract
Objective:
A major consequence of acute myocardial infarction is myocardial ischemia-reperfusion (I/R) injury. Collecting proof demonstrates that AXIN1 assume a basic part in different disease; however, the role of AXIN1 in I/R injury remains to a great extent obscure.
Methods:
The I/R injury model on AC16 cells was constructed. siRNA transfection was used to knockdown AXIN1. The qRT-PCR assays and western blot assays were used to detect the expression level of AXIN1 and other key proteins. CCK-8 assays and cell apoptosis assays were used to detect cell proliferation and cell apoptosis.
Results:
AXIN1 was significantly overexpressed in an in vitro model of I/R injury. Knockdown of AXIN1 significantly restored the cell proliferation inhibition caused by IR injury, while inhibiting apoptosis and inflammation. Further mechanistic studies revealed that the transcription factor c-Myc could regulate the expression of AXIN1. The effects of I/R injury on AC16 cells after overexpression of c-Myc were reversed by knockdown of AXIN1. Meanwhile, AXIN1 could regulate the SIRT1/p53/Nrf 2 pathway.
Conclusion:
Our results show an important role for AXIN1 and provide new targets for avoiding and treating I/R injury.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Reference31 articles.
1. China cardiovascular diseases report 2015: a summary;Chen;J Geriatr Cardiol,2017
2. Outline of the report on cardiovascular diseases in China, 2014;Weiwei;Eur Heart J Suppl,2016
3. China cardiovascular diseases report 2018: an updated summary;Ma;J Geriatr Cardiol,2020
4. Myocardial ischemia-reperfusion injury: a neglected therapeutic target;Hausenloy;J Clin Invest,2013
5. Remote ischemic conditioning in acute myocardial infarction and shock states;Kloner;J Cardiovasc Pharmacol Ther,2020