Long non-coding RNA HOTAIR promotes LPS-induced inflammatory injury by down-regulation of microRNA-124 in murine chondrogenic ATDC5 cells

Publication date: Available online 20 July 2018Source: Life SciencesAuthor(s): Guoqing Duan, Shiqiang Song, Shuaishuai NiuAbstractAimsLong non-coding RNAs (lncRNAs) exert important functions in pathogenesis of osteoarthritis (OA). Our study aimed to explore the effects of lncRNA HOX transcript antisense RNA (HOTAIR) on LPS-induced inflammatory injury in ATDC5 cells, as well as potential mechanism(s).Main methodsHOTAIR expression was measured in both OA patients and non-OA patients. ATDC5 cells were treated with LPS and/or transfected with pc-HOTAIR, sh-HOTAIR, miR-124 mimic and their corresponding negative controls. The expression of HOTAIR, matrix metalloproteinase (MMP)-1, MMP-13 and miR-124 was detected by qRT-PCR. Cell viability and cell apoptosis were assessed by CCK-8 assay and flow cytometry, respectively. The protein expression was detected by western blot.Key findingsHOTAIR expression was significantly up-regulated in OA patients (P < 0.01). LPS statistically decreased cell viability while significantly increased cell apoptosis and expression of MMP-1, MMP-13 and HOTAIR in ATDC5 cells (P < 0.05 or P < 0.01). HOTAIR overexpression significantly decreased cell viability while statistically increased cell apoptosis and expression of MMP-1 and MMP-13 (P < 0.05 or P < 0.01). HOTAIR knockdown led the opposite results. In addition, HOTAIR negatively regulated expression of miR-124 (P < 0.05). Co-transfection of miR-124 mimic a...
Source: Life Sciences - Category: Biology Source Type: research