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MiR‐20a inhibits the progression of human arthritis fibroblast‐like synoviocytes and inflammatory factor expression by targeting ADAM10
MiR‐20a has been reported as a key regulator to pro‐inflammatory factor release in fibroblast‐like synoviocytes (FLS), which caused rheumatoid arthritis (RA). However, the molecular mechanism of miR‐20a in RA remains to be further elucidated. This study aimed to investigate the roles of miR‐20a in RA pathology. RA (n = 24) and osteoarthritis (OA, n = 20) and normal healthy tissues (n = 16) were collected from operation. TargetScan and dual‐luciferase reporter were performed to predict and confirm the potential binding sites of miR‐20a on ADAM metallopeptidase domain 10 (ADAM10). Pearson's analysis was adopted to evaluate the correlation between miR‐20a and ADAM10 expression. It was found that MiR‐20a was downregulated in RA tissues, and overexpressed miR‐20a inhibited cell viability, migration and invasion, and the expression of inflammatory factors in RA‐FLS MH7A cells. ADAM10 was identified as the target gene of miR‐20a, and upregulation of ADAM10 reversed the inhibitory effects of miR‐20a. In conclusion, miR‐20a inhibits the progression of RA‐FLS as well as the inflammatory factor expression by targeting ADAM10.
MiR‐20a inhibits the progression of human arthritis fibroblast‐like synoviocytes and inflammatory factor expression by targeting ADAM10
MiR‐20a has been reported as a key regulator to pro‐inflammatory factor release in fibroblast‐like synoviocytes (FLS), which caused rheumatoid arthritis (RA). However, the molecular mechanism of miR‐20a in RA remains to be further elucidated. This study aimed to investigate the roles of miR‐20a in RA pathology. RA (n = 24) and osteoarthritis (OA, n = 20) and normal healthy tissues (n = 16) were collected from operation. TargetScan and dual‐luciferase reporter were performed to predict and confirm the potential binding sites of miR‐20a on ADAM metallopeptidase domain 10 (ADAM10). Pearson's analysis was adopted to evaluate the correlation between miR‐20a and ADAM10 expression. It was found that MiR‐20a was downregulated in RA tissues, and overexpressed miR‐20a inhibited cell viability, migration and invasion, and the expression of inflammatory factors in RA‐FLS MH7A cells. ADAM10 was identified as the target gene of miR‐20a, and upregulation of ADAM10 reversed the inhibitory effects of miR‐20a. In conclusion, miR‐20a inhibits the progression of RA‐FLS as well as the inflammatory factor expression by targeting ADAM10.
MiR‐20a inhibits the progression of human arthritis fibroblast‐like synoviocytes and inflammatory factor expression by targeting ADAM10
Xie, Zikang (author) / Shen, Pengfei (author) / Qu, Yuxing (author) / Xu, Jianda (author) / Zheng, Chong (author) / Gao, Yi (author) / Wang, Bin (author)
Environmental Toxicology ; 35 ; 867-878
2020-08-01
12 pages
Article (Journal)
Electronic Resource
English
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