LncRNA SRA deregulation contributes to the development of atherosclerosis by causing dysfunction of endothelial cells through repressing the expression of adipose triglyceride lipase.

LncRNA SRA deregulation contributes to the development of atherosclerosis by causing dysfunction of endothelial cells through repressing the expression of adipose triglyceride lipase.
Mol Med Rep. 2018 Sep 20;:
Authors: Yang S, Sun J
Abstract
It has been well established that long non‑coding RNAs (lncRNAs) are crucial mediators in a diverse range of diseases, including atherosclerosis. The present study aimed to examine the molecular mechanisms underlying the association between steroid receptor RNA activator (SRA) and atherosclerosis. Reverse transcription‑quantitative polymerase chain reaction analysis, western blot analysis and luciferase assays were performed to examine interactions among SRA, adipose triglyceride lipase (ATGL) and peroxisome proliferator‑activated receptor (PPARγ), and the effect of resveratrol (RSV) on the levels of SRA, ATGL and PPARγ. ELISA was performed to determine the effects of SRA and RSV on the production of inflammatory‑associated cytokines. The results showed that knockdown of the expression of SRA by transfecting HUVECs with short hairpin RNA‑SRA inhibited the production of ATGL and PPARγ. A plasmid coding SRA RNA, but not the SRAP protein, attenuated the luciferase activity of the ATGL promoter. PPARγ had no effect on the luciferase activity driven by the ATGL promoter in the absence of rosiglitazone, whereas the luciferase activity of the ATGL promoter was elevated in the presence of ...

Source: Molecular Medicine Reports - October 3, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research