Open AccessmiRNA‑27a regulates arthritis via PPARγ in�vivo and in�vitro
Author(s) -
Yu Xiao,
Bing Li,
Jun Li
Publication year - 2018
Publication title -
molecular medicine reports
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2018.8531
Subject(s) - arthritis , downregulation and upregulation , in vivo , peroxisome proliferator activated receptor , inflammation , cancer research , oncogene , microrna , inflammatory arthritis , in vitro , chemistry , alkaline phosphatase , endocrinology , apoptosis , medicine , receptor , biology , cell cycle , biochemistry , enzyme , microbiology and biotechnology , gene
The present study investigated the role of microRNA (miR)‑27a in the development of arthritis and its mechanism of action. Initially, collagen was used to develop an in vivo rat model of arthritis. Changes in the miRs in the rats were analyzed. It was subsequently observed that miR‑27a expression was reduced in patients with arthritis, compared with the control group. In the present study an in vitro miR‑27a overexpression model of arthritis was established and it was observed that miR‑27a increased the proliferation of osteoblast‑like cells in vitro. miR‑27a overexpression promoted osteogenic differentiation, increased alkaline phosphatase (ALP) and osteoporosis (OST) content, induced insulin‑like growth factor binding protein-5 (IGFBP‑5) protein expression, reduced inflammation and suppressed peroxisome proliferator‑activated receptor γ (PPARγ) and matrix metalloproteinase-17 (MMP‑17) protein expression in arthritis. However, miR‑27a downregulation inhibited osteogenic differentiation, increased inflammation and PPARγ and MMP‑17 protein expression and suppressed ALP and OST content in an in vitro model of arthritis. The PPARγ inhibitor reduced the function of miR‑27a downregulation on arthritis. Therefore the results of the present study revealed that miR‑27a regulates arthritis via PPARγ.