Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MiR-498 suppresses proliferation and inflammation in fibroblast-like synoviocytes in rheumatoid arthritis via targeting JAK1

Lan Chai¹, Xian Zhen Zhang² , Hai fang Ma³, Fang Yuan¹

¹Department of Rheumatology and Immunology, Zhejiang Hospital; ²Department of Rheumatology, Tongde Hospital of Zhejiang Province; ³Department of Clinical Laboratory, Zhejiang Hospital, Hang Zhou City, Zhe Jiang Province 310000, China.

For correspondence:- Xian Zhang Email: XianZhengZhang125@163.com Tel:+8657189972412

Accepted: 28 September 2019 Published: 30 October 2019

Citation: Chai L, Zhang XZ, Ma Hf, Yuan F. MiR-498 suppresses proliferation and inflammation in fibroblast-like synoviocytes in rheumatoid arthritis via targeting JAK1. Trop J Pharm Res 2019; 18(10):2011-2017 doi: 10.4314/tjpr.v18i10.2

© 2019 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of microRNA 498 (miR-498) on proliferation and inflammation of rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLSs) in rheumatoid arthritis (RA).

Methods: MiR-498 level was evaluated in both RA synovial tissues and RA-FLSs using real-time polymerase chain reaction (PCR). MicroRNA-498 overexpression or knockdown was performed in RA-FLSs. Proliferation, apoptosis, cell cycle and inflammation induced by miR-498 mimics or inhibitor were used to explore the function of miR-498 in RA.

Results: expression level of miR-498 was downregulated in both RA synovial tissues and RA- FLSs. MicroRNA-498 mimics decreased proliferation and arrested cell cycle, whereas miR-498 inhibitor caused the opposite effects in RA-FLSs. In addition, miR-498 mimics suppressed inflammation and promoted cell apoptosis, while miR-498 inhibitor promoted inflammation and inhibited cell apoptosis in RA-FLSs. Furthermore, the effect of miR-498 on the proliferation, inflammation and apoptosis of RA-FLSs was mediated by its ability to target and downregulate JAK1.

Conclusion: These results indicate that miR-498 inhibits the proliferation and inflammatory responses of RA-FLSs by targeting JAK1, thus revealing a new therapeutic target for RA treatment.

Keywords: Rheumatoid arthritis, MiR-498, JAK1, Proliferation, Inflammation