LincRNA00612 inhibits apoptosis and inflammation in LPS-induced BEAS-2B cells via enhancing interaction between p-STAT3 and A2M promoter

PeerJ

article

Xinru Xiao¹  Wei Cai¹  Ziqi Ding¹  Zhengdao Mao¹  Yujia Shi¹  Qian Zhang¹ 

[1] Department of Respiratory and Critical Care Medicine, The Affiliated Changzhou No. 2 People’s Hospital of Nanjing Medical University;Department of the Second Clinical College, Dalian Medical University

关键词: LINC00612;    Chronic obstructive pulmonary disease;    Alpha-2-macroglobulin;    Signal transducer and activator of transcription 3;   

DOI  :  10.7717/peerj.14986

学科分类：社会科学、人文和艺术（综合）

来源: Inra

【 摘 要 】

Long non-coding RNAs (lncRNAs) have been reported as key regulators of chronic obstructive pulmonary disease (COPD). This study aimed to figure out the regulatory mechanism as well as the effects of lncRNA00612 (LINC00612) in lipopolysaccharide (LPS)-induced inflammation and apoptosis in BEAS-2B cells. LINC00612 and its co-expressed gene alpha-2-macroglobulin (A2M) were strikingly downregulated in the peripheral venous blood of COPD patients. Overexpressed LINC00612 enhances BEAS-2B cells against apoptosis and inflammatory reactions mediated by LPS, however, an A2M knockdown can attenuate the degree of the enhancement. Bioinformatics analysis revealed putative binding sites between LINC00612, signal transducer and activator of transcription 3 (STAT3) and the A2M promoter, while RNA antisense purification and Chromatin immunoprecipitation were performed to confirm the prediction. Knockdown of LINC00612 impaired the binding of p-STAT3 to the promoter of A2M, which meant that LINC00612 was critical for the binding of STAT3 with the A2M promoter. Therefore, it can be concluded that LINC00612 ameliorates LPS-induced cell apoptosis and inflammation via recruiting STAT3 to bind to A2M. This conclusion will serve as a theoretical foundation for the treatment of COPD.

【 授权许可】

CC BY