Abstract
Purpose: To investigate the effect of miR-493-5p in lipopolysaccharide (LPS) -induced ATDC5 chondrogenic cells.
 Methods: The MTT assay was used to determine the viability of LPS-induced ATDC5 cells. ENCORI (starbase.sysu.edu.cn/) was used to predict the target of miR-493-5p. Quantitative reverse-transcription-polymerase chain reaction (qRT-PCR) was used to determine miR-493-5p expression in ATDC5 controlled cells and cells treated with various combinations of LPS, negative control miRNA (NC), miR-493-5p mimic, TAB2 overexpression vector, and miR-493-5p inhibitor. qRT-PCR, while western blot was used to assess TAB2 mRNA and protein expression levels in control, LPS, LPS + NC, LPS + miR-493-5p mimic, and LPS + miR-493-5p inhibitor groups. The qRT-PCR and ELISA were used to evaluate TNF-α, IL-18, and IL-1β expressions in control, NC, LPS, LPS + NC, miR-493-5p mimic, and LPS + miR-493-5p mimic. Furthermore, the two techniques were also used determine LPS + miR-493-5p inhibitor, LPS + TAB2 overexpression, and LPS + TAB2 overexpression + miR-493-5p mimic groups.
 Results: MiR-493-5p expression was downregulated in LPS-induced ATDC5 cells (p < 0.001). Overexpression of miR-493-5p increased LPS-induced ATDC5 cell viability but decreased expression of inflammatory factors (p < 0.001). MiR-493-5p targeted and inhibited TAB2 expression in LPS-induced ATDC5 cells (p < 0.001). TAB2 overexpression reversed the suppression of TAB2 by miR-493-5p in LPS-induced ATDC5 cell injury (p < 0.001).
 Conclusion: MiR-493-5p alleviates LPS-induced inflammation of ATDC5 chondrogenic cells by targeting TAB2. Thus, miR-493-5p and TAB2 have potentials for use as clinical therapeutic targets for OA.
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