Zhe Ni1, Xifu Shang2, Guolin Tang2, Lei Niu2. 1. Department of Orthopedics, Anhui Provincial Hospital, Hefei, Anhui, China. Electronic address: zhenini@yeah.net. 2. Department of Orthopedics, Anhui Provincial Hospital, Hefei, Anhui, China.
Abstract
BACKGROUND: Increasing evidence has demonstrated that microRNAs regulate the development of cartilage and osteogenesis. Whether miR-206 participates in the development of human articular cartilage remains largely unknown. This study aimed to investigate the role of miR-206 in human chondrocytes. METHODS: Expression of miR-206 was initially assessed in human osteoarthritis (OA) tissues and articular chondrocytes through quantitative real-time polymerase chain reaction. The effects of miR-206 on proliferation and apoptosis of human chondrocytes were assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining assay. Then, the effects of miR-206 on type II collagen alpha 1 (Col2a1), aggrecan, runt-related transcription factor 2 (RUNX2) and matrix metalloproteinase13 (MMP13) were examined with quantitative real-time polymerase chain reaction and Western blot analysis. RESULTS: MiR-206 was significantly increased in human OA tissues and chondrocytes. MiR-206 significantly inhibited the proliferation of chondrocytes, but promoted apoptosis. Expression of Col2a1 and aggrecan were dramatically decreased, and the expression of RUNX2 and MMP13 were significantly increased when miR-206 was overexpressed. CONCLUSIONS: MiR-206 may participate in cartilage degradation in OA. Manipulation of the expression of miR-206 in human chondrocytes may be a novel therapeutic strategy for the treatment of OA.
BACKGROUND: Increasing evidence has demonstrated that microRNAs regulate the development of cartilage and osteogenesis. Whether miR-206 participates in the development of humanarticular cartilage remains largely unknown. This study aimed to investigate the role of miR-206 in human chondrocytes. METHODS: Expression of miR-206 was initially assessed in humanosteoarthritis (OA) tissues and articular chondrocytes through quantitative real-time polymerase chain reaction. The effects of miR-206 on proliferation and apoptosis of human chondrocytes were assessed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) and Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining assay. Then, the effects of miR-206 on type II collagen alpha 1 (Col2a1), aggrecan, runt-related transcription factor 2 (RUNX2) and matrix metalloproteinase13 (MMP13) were examined with quantitative real-time polymerase chain reaction and Western blot analysis. RESULTS:MiR-206 was significantly increased in human OA tissues and chondrocytes. MiR-206 significantly inhibited the proliferation of chondrocytes, but promoted apoptosis. Expression of Col2a1 and aggrecan were dramatically decreased, and the expression of RUNX2 and MMP13 were significantly increased when miR-206 was overexpressed. CONCLUSIONS:MiR-206 may participate in cartilage degradation in OA. Manipulation of the expression of miR-206 in human chondrocytes may be a novel therapeutic strategy for the treatment of OA.
Authors: Rodrigo Coutinho de Almeida; Yolande F M Ramos; Ahmed Mahfouz; Wouter den Hollander; Nico Lakenberg; Evelyn Houtman; Marcella van Hoolwerff; H Eka D Suchiman; Alejandro Rodríguez Ruiz; P Eline Slagboom; Hailiang Mei; Szymon M Kiełbasa; Rob G H H Nelissen; Marcel Reinders; Ingrid Meulenbelt Journal: Ann Rheum Dis Date: 2018-12-01 Impact factor: 19.103