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微小 RNA-31 通过靶向 C-X-C 基序趋化因子配体 12 促进软骨细胞增殖。

MicroRNA‑31 promotes chondrocyte proliferation by targeting C‑X‑C motif chemokine ligand 12.

机构信息

Department of Orthopedics, The Affiliated Huai'an Hospital of Xuzhou Medical University and The Second People's Hospital of Huai'an, Huai'an, Jiangsu 223200, P.R. China.

Department of Orthopedics, Huai'an Hospital of Traditional Chinese Medicine, Huai'an, Jiangsu 223200, P.R. China.

出版信息

Mol Med Rep. 2019 Mar;19(3):2231-2237. doi: 10.3892/mmr.2019.9859. Epub 2019 Jan 15.

Abstract

The present study aimed to investigate the biological function and underlying molecular mechanisms of miR-31 in osteoarthritis (OA). Reverse transcription‑quantitative polymerase chain reaction was used to detect miR‑31 expression, and it was found that miR‑31 was downregulated in the cartilage tissues of OA patients. microRNA.org was used to predict the gene targets of miR‑31, and dual luciferase reporter assays were used to verify that C‑X‑C motif chemokine ligand 12 (CXCL12) was a direct target of miR‑31. The human chondrocyte cell line CHON‑001 was used to perform MTT and cell migration assays. Western blotting was used to measure the protein expression of CXCL12, type I collagen and aggrecan. The results suggested that CXCL12 was a target of miR‑31, and the expression of CXCL12 was negatively regulated by miR‑31 in CHON‑001 cells. miR‑31 increased CHON‑001 cell viability and migration, as well as the expression of type I collagen and aggrecan. Furthermore, the overexpression of CXCL12 eliminated the effects of miR‑31 mimics on CHON‑001 cells. In conclusion, the data indicated that miR‑31 promoted chondrocyte viability and migration by directly targeting CXCL12, which provided evidence for CXCL12 as a potential target in OA therapy.

摘要

本研究旨在探讨 miR-31 在骨关节炎(OA)中的生物学功能及其潜在的分子机制。逆转录-定量聚合酶链反应用于检测 miR-31 的表达,结果发现 miR-31 在 OA 患者的软骨组织中下调。microRNA.org 用于预测 miR-31 的基因靶标,双荧光素酶报告基因实验用于验证 C-X-C 基元趋化因子配体 12(CXCL12)是 miR-31 的直接靶标。使用人软骨细胞系 CHON-001 进行 MTT 和细胞迁移实验。Western blot 用于测量 CXCL12、I 型胶原和聚集蛋白聚糖的蛋白表达。结果表明,CXCL12 是 miR-31 的靶标,并且在 CHON-001 细胞中,CXCL12 的表达受 miR-31 的负调控。miR-31 增加了 CHON-001 细胞的活力和迁移,以及 I 型胶原和聚集蛋白聚糖的表达。此外,CXCL12 的过表达消除了 miR-31 模拟物对 CHON-001 细胞的影响。综上所述,数据表明 miR-31 通过直接靶向 CXCL12 促进软骨细胞的活力和迁移,为 CXCL12 作为 OA 治疗的潜在靶点提供了证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/13df/6390014/44b6980d0e12/MMR-19-03-2231-g00.jpg

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