基因沉默
炎症
丝氨酸蛋白酶
小发夹RNA
败血症
小干扰RNA
化学
癌症研究
基因表达
基因敲除
信使核糖核酸
丝氨酸
蛋白酶
细胞生物学
核糖核酸
医学
生物
免疫学
基因
生物化学
磷酸化
酶
作者
Wei Xie,Anqi Zhang,Xinghui Huang,Hui Zhou,Hangbo Ying,Changzhou Ye,Ran Miao,Meizi Qian,Xia Liu,Yunchang Mo
出处
期刊:Shock
[Ovid Technologies (Wolters Kluwer)]
日期:2023-03-07
卷期号:59 (5): 791-802
被引量:3
标识
DOI:10.1097/shk.0000000000002106
摘要
Sepsis-induced cardiomyopathy (SIC) is one of the most common complications of infection-induced sepsis. An imbalance in inflammatory mediators is the main factor leading to SIC . N 6 -methyladenosine (m 6 A) is closely related to the occurrence and development of sepsis. N 6 -methyladenosine reader YTH domain containing 1 (YTHDC1) is an m 6 A N 6 -methyladenosine recognition protein. However, the role of YTHDC1 in SIC remains unclear. Herein, we demonstrated that YTHDC1-shRNA inhibits inflammation, reduces inflammatory mediators, and improves cardiac function in a LPS-induced SIC mouse model. Based on the Gene Expression Omnibus database analysis, serine protease inhibitor A3N is a differential gene of SIC. Furthermore, RNA immunoprecipitation indicated that serine protease inhibitor A3N (SERPINA3N) mRNA can bind to YTHDC1, which regulates the expression of SERPINA3N. Serine protease inhibitor A3N-siRNA reduced LPS-induced inflammation of cardiac myocytes. In conclusion, the m 6 A reader YTHDC1 regulates SERPINA3N mRNA expression to mediate the levels of inflammation in SIC. Such findings add to the relationship between m 6 A reader YTHDC1 and SIC, providing a new research avenue for the therapeutic mechanism of SIC.
科研通智能强力驱动
Strongly Powered by AbleSci AI