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

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 tiss...

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Detalles Bibliográficos
Autores principales: Dai, Yankun, Liu, Shanglun, Xie, Xueguan, Ding, Mingsheng, Zhou, Quan, Zhou, Xiaoqing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390014/
https://www.ncbi.nlm.nih.gov/pubmed/30664157
http://dx.doi.org/10.3892/mmr.2019.9859
Descripción
Sumario: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.