All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Abstract

Inhibition of miR-5571-3p Attenuates Proliferation and Invasion in Rheumatoid Arthritis Fibroblast-like Synoviocytes by Upregulating OAZ3

Author(s): J. LIN*, B. X. LIU AND H. M. ZOU
Department of Rheumatology and Immunology, Taizhou People’s Hospital, No. 366 Taihu Road, Taizhou, Jiangsu 225300, China

Correspondence Address:
Department of Rheumatology and Immunology, Taizhou People’s Hospital, No. 366 Taihu Road, Taizhou, Jiangsu 225300, China, E-mail: [email protected]

The aim of the present study was to explore the role and potential mechanism of miR-5571-3p in rheumatoid arthritis. In this study, miR-5571-3p level in rheumatoid arthritis tissues and fibroblast-like synoviocytes was detected using qRT-PCR analysis. Cell Counting Kit-8 assay was performed to determine proliferation of fibroblast-like synoviocyte. Transwell assay was conducted to examine the invasion of fibroblast-like synoviocytes, and western blot analysis was used to examine the ornithine decarboxylase antizyme 3 protein expression. Results showed that miR-5571-3p expression was elevated in vivo and in vitro in rheumatoid arthritis. Inhibition of miR-5571-3p suppressed rheumatoid arthritis fibroblastlike synoviocyte proliferation and invasion. ornithine decarboxylase antizyme 3 siRNA could partially abolish the suppressor effect of miR-5571-3p inhibitor in cell proliferation and invasion in fibroblastlike synoviocytes. In conclusion, miR-5571-3p and ornithine decarboxylase antizyme 3 played important regulatory roles in proliferation and invasion of rheumatoid arthritis fibroblast-like synoviocytes, miR5571-3p/ornithine decarboxylase antizyme 3 axis could serve as a new target for therapy of rheumatoid arthritis.

Full-Text | PDF