LncRNA H19 inhibitor represses synovial cell proliferation and apoptosis in rats with rheumatoid arthritis via Notch signaling pathway.

Abstract

To study the roles and underlying mechanisms of long non-coding ribonucleic acid (lncRNA) H19 in the synovial cell proliferation and apoptosis in rats with rheumatoid arthritis (RA). A total of 30 Sprague-Dawley rats were randomly divided into Control group and Model group. The rat model of RA was induced by using type II collagen in Model group. The primary synovial cells were isolated from the synovial tissues of the rats and were assigned into Control group, Model group, and lncRNA H19 inhibitor intervention group. 5-Ethynyl-2'-deoxyuridine (EdU) staining was applied to detect cell proliferation in each group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was employed to determine the cell apoptosis in each group. Western blotting assay was adopted to measure the expression levels of Notch1 and hairy/enhancer of split-1 (Hes1) in each group of cells. The RA score of the Model group was higher than that of the Control group. Compared to the Control group, the expression of lncRNA H19, Notch, and Hes1 of the synovial cells in the Model group were significantly elevated. Besides, the cell proliferation rate of the Model was also increased, while the cell apoptosis rate was decreased compared with those in the Control group. Moreover, in comparison with Model group, lncRNA H19 inhibitor intervention group exhibited a lowered lncRNA H19 level, remarkably reduced cell proliferation rate and protein levels of Notch1 and Hes1, as well as notably raised cell apoptosis rate. Our results indicated that lncRNA H19 inhibitor could repress the proliferation and promote the apoptosis of synovial cells in RA rats, which might be attributed to the inhibition of the Notch signaling pathway.