Knockdown of MFI2-AS1 increased cell viability but suppressed apoptosis, inflammatory response and extracellular matrix degradation in LPS-treated chondrocytes by increasing miR-130a-3p and decreasing TCF4, indicating a novel target for the treatment of osteoarthritis.
LncRNA H19 aggravated the injury of LPS-induced C28/I2 cells by sponging miR-130a, hinting a novel regulatory mechanism and a potential therapeutic target for OA.
Our results indicated that miR-130a played an important role in regulating the expression of TNF-α in human chondrocytes and identified miR-130a as a novel therapeutic target in OA.