SNHG6 modulates oxidized low-density lipoprotein-induced endothelial cells injury through miR-135a-5p/ROCK in atherosclerosis.

BACKGROUND

Plenty of long non-coding RNAs (lncRNAs) play vital roles in the progression of atherosclerosis. Small nucleolar RNA host gene 6 (SNHG6) is a well known lncRNA that is aberrantly high expressed in atherosclerosis patients. However, its function and basic mechanism in atherosclerosis events have not been well clarified.

METHODS

The expression patterns of SNHG6, miR-135a-5p, ROCK1 and ROCK2 in clinical samples and cells were detected by RT-qPCR assays. Cell Counting Kit-8 (CCK-8), flow cytometry assays, ELISA and reactive oxygen species (ROS) and malondialdehyde (MDA) detection, were performed to assess cell viability, apoptosis, inflammation and oxidative stress, respectively. Western blot analysis was carried out to examine the protein levels of Bax, Bcl-2, and SNHG6. Luciferase reporter and RIP assays were used to confirm the true interaction between SNHG6 and miR-135a-5p, or miR-135a-5p and ROCK.

RESULTS

The levels of SNHG6, ROCK1 and ROCK2 were notably increased and miR-135a-5p was decreased in atherosclerosis patients and oxidized low-density lipoprotein (ox-LDL)-treated HUVECs. Knockdown of SNHG6 alleviated ox-LDL-induced injury of HUVECs, while this effect was partly reversed by miR-135a-5p inhibitor. Moreover, overexpression of ROCKs aggravated miR-135a-5p-alleviated atherosclerosis cell injury. SNHG6 contributed to ROCK expression through sequestering miR-135a-5p as a molecular sponge.

CONCLUSION

SNHG6 functions as a promoter in atherosclerosis events by targeting miR-135a-5p/ROCK axis in ox-LDL-stimulated HUVECs. This finding will help to develop a novel therapeutic strategy for atherosclerosis.