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miR-590 在类风湿关节炎中的上调通过转化生长因子-β1/磷脂酰肌醇 3-激酶/蛋白激酶 B 信号通路促进破骨细胞凋亡。

Upregulation of microRNA‑590 in rheumatoid arthritis promotes apoptosis of bone cells through transforming growth factor‑β1/phosphoinositide 3‑kinase/Akt signaling.

机构信息

Department of Orthopedics and Traumatology, Yuxi Municipal Hospital of Traditional Chinese Medicine, Yuxi, Yunnan 653100, P.R. China.

出版信息

Int J Mol Med. 2019 May;43(5):2212-2220. doi: 10.3892/ijmm.2019.4116. Epub 2019 Feb 28.

Abstract

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.

摘要

本研究旨在进一步明确微小 RNA(miR)-590 在骨关节炎(OA)中的作用,并探讨其潜在机制。简而言之,采用逆转录-定量聚合酶链反应分析 OA 大鼠骨组织样本中 miR-590 的表达。结果表明 miR-590 的表达上调。miR-590 上调诱导骨细胞凋亡,而 miR-590 下调则减少骨细胞凋亡。此外,miR-590 上调抑制骨细胞中转化生长因子(TGF)-β1、磷酸肌醇 3-激酶(PI3K)和磷酸化(p)-Akt 的蛋白表达水平。然而,miR-590 下调诱导骨细胞中 TGF-β1、PI3K 和 p-Akt 的蛋白表达水平升高。此外,TGF-β1 减弱了 miR-590 上调对骨细胞凋亡的影响,而 PI3K 抑制剂抑制了 miR-590 下调对骨细胞凋亡的影响。综上所述,这些数据表明 miR-590 通过调节 TGF-β1/PI3K 信号通路促进 OA 大鼠骨细胞凋亡。

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