Long non-coding RNA FOXD3-AS1 aggravates ischemia/reperfusion injury of cardiomyocytes through promoting autophagy.

作者：Guoxin Tong, Yongmei Wang, Chenke Xu, Yizhou Xu, Xianhua Ye, Liang Zhou, Gangjie Zhu, Zhan-lin Zhou, Jinyu Huang · 发表于：PubMed · 年份：2019 · 被引用次数：31 · 研究领域：Cancer-related molecular mechanisms research、Autophagy in Disease and Therapy、Cardiac Ischemia and Reperfusion

We aimed to investigate the role of long non-coding RNA (lncRNA) FOXD3 antisense RNA 1 (FOXD3-AS1) in myocardial Ischemia/reperfusion (I/R) injury. In our study, H9C2 cells were treated with oxygen-glucose deprivation and reoxygenation (OGD/R). RT-qPCR was performed to detect the expression level of lncRNA FOXD3-AS1 in OGD/R induced H9C2 cells. Then, pcDNA-lncRNA FOXD3-AS1 was transfected into H9C2 cells. The level of LC3 II was measured by immunofluorescence assay. And the expression of autophagy related genes were detected using western blot. In addition, 3-methyladenine (3 M), an autophagy inhibitor, was recruited to treat with H9C2 cells. The contents of creatine kinase (CK), CK isoenzymes (CK-MB), cardiac troponin I (cTnI), inflammation associated factors, reactive oxygen (ROS) and NO were evaluated by kits. Moreover, cell apoptosis was measured by a flow cytometry assay and the expression levels of apoptosis associated proteins were evaluated by western blot. Furthermore, the expression of NF-κB/iNOS/COX2 signaling were measured in our study. The results indicated that FOXD3-AS1 expression was increased in OGD/R-treated H9C2 cells and overexpression of FOXD3-AS1 upregulated the expression of LC3 II, Beclin1, ATG5 accompanied by a downregulated expression of p62. In addition, FOXD3-AS1 overexpression increased the levels of CK, CK-MB, cTnI, TNF-α, IL-1β, IL-6, ROS and NO, whereas the increase of above factors were reversed following treatment with 3 M. Moreover, FOXD3-AS...