Open AccessUpregulation of microRNA‑590 in rheumatoid arthritis promotes apoptosis of bone cells through transforming growth factor‑β1/phosphoinositide 3‑kinase/Akt signaling
Author(s) -
Jun Young Yang,
Yunxiang Zhuang,
Jianghua Liu
Publication year - 2019
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2019.4116
Subject(s) - downregulation and upregulation , pi3k/akt/mtor pathway , protein kinase b , apoptosis , phosphoinositide 3 kinase , microbiology and biotechnology , cancer research , transforming growth factor , signal transduction , chemistry , biology , biochemistry , gene
The aim of the present study was to further define the role of microRNA (miR)‑590 in osteoarthritis (OA) and to investigate the underlying mechanism. In brief, reverse transcription‑quantitative polymerase chain reaction was used to analyze miR‑590 expression in bone tissue samples from rats with OA. Results indicated the expression of miR‑590 was increased. miR‑590 upregulation induced apoptosis in bone cells, whereas miR‑590 downregulation reduced apoptosis of bone cells. Furthermore, miR‑590 upregulation suppressed the protein expression levels of transforming growth factor (TGF)‑β1, phosphoinositide 3‑kinase (PI3K) and phosphorylated (p)‑Akt in bone cells. However, downregulation of miR‑590 induced the protein expression levels of TGF‑β1, PI3K and p‑Akt in bone cells. In addition, TGF‑β1 attenuated the effects of miR‑590 upregulation on bone cell apoptosis and the inactivation of PI3K inhibited the effects of miR‑590 downregulation on bone cell apoptosis. Taken together, the present data suggested that miR‑590 promoted apoptosis in bone cells from rats with OA by regulating the TGF‑β1/PI3K signaling pathway.