Upregulation of miR-98 Inhibits Apoptosis in Cartilage Cells in Osteoarthritis

• Published in: Genetic testing and molecular biomarkers Vol. 20; no. 11; p. 645
• Main Authors: Wang, Gui-Long, Wu, Yu-Bo, Liu, Jia-Tian, Li, Cui-Yun
• Format: Journal Article
• Language: English
• Published: United States 01.11.2016
• Subjects: Adult; Aged; Animals; Apoptosis - genetics; Cartilage - metabolism; Cartilage - pathology; Chondrocytes - metabolism; Chondrocytes - pathology; Disease Models, Animal; Female; Humans; Male; MicroRNAs - genetics; MicroRNAs - metabolism; Middle Aged; Osteoarthritis, Knee - genetics; Osteoarthritis, Knee - metabolism; Osteoarthritis, Knee - pathology; Rats; Rats, Sprague-Dawley; RNA, Messenger - genetics; RNA, Messenger - metabolism; RNA, Small Interfering - genetics; Up-Regulation; cartilage cells; TUNEL assay; osteoarthritis; Annexin V-PI double staining assay; apoptosis; siRNA; miR-98
• DOI: 10.1089/gtmb.2016.0011

We aimed to investigate the effects of microRNA-98 (miR-98) on apoptosis in cartilage cells of osteoarthritis (OA) patients. Knee cartilage tissue samples were collected from 31 OA patients, 21 autopsies, and 26 amputation patients due to trauma. The clinicopathological data were recorded. Quantitative real-time polymerase chain reaction was performed to compare the miR-98 expression levels from cartilage cells obtained from the OA and non-OA patients. Clinicopathological characteristics of the patients were also analyzed. Primary chondrocytes were separated from cartilage tissues and transfected with plasmids or siRNA to overexpress or inhibit miR-98. Annexin V-PI double staining and TUNEL assays were used to examine apoptosis in the primary chondrocytes after transfection. Finally, a rat OA model was used to confirm the effects of miR-98 on apoptosis in cartilage cells in vivo. Compared with the normal cartilage tissues, miR-98 expression was reduced in the OA cartilage tissues (p < 0.01). The miR-98 expression levels were also significantly correlated with the OA stage (p < 0.05). In vitro, transfection with the miR-98 inhibitor increased apoptosis in the cartilage cells (p < 0.05), and transfection with a miR-98 mimic inhibited apoptosis in cartilage cells (p < 0.05). In the OA rat model, exogenous injection of the miR-98 mimic inhibited apoptosis in the rat cartilage cells thus alleviating OA. MiR-98 expression is reduced in the cartilage cells of OA patients and the overexpression of miR-98 inhibits cartilage cell apoptosis, while inhibition of microRNA-98 leads to cartilage cell apoptosis. These findings provide a theoretical basis for the development of novel targeted therapies for OA.