MiR‐22 restrains proliferation of rheumatoid arthritis by targeting IL6R and may be concerned with the suppression of NF‐κB pathway

• Main Authors: Qing‐Yi Yang, Kai‐Peng Yang, Zhi‐Zhou Li
• Format: Article
• Language: English
• Published: Wiley 2020-01-01
• Series: Kaohsiung Journal of Medical Sciences
• Subjects: fibroblast‐like synoviocytes; IL6R; inflammatory injury; miR‐22; NF‐κB signaling pathway; rheumatoid arthritis
• Online Access: https://doi.org/10.1002/kjm2.12124
• ISSN: 1607-551X; 2410-8650

Abstract It has demonstrated that miR‐22 overexpression can suppress the inflammation process of rheumatoid arthritis (RA) in synoviocytes. But, the underlying mechanism of miR‐22 expression in regulating RA is still not well illustrated. In this study, we investigated the functional role and underlying mechanism of miR‐22 in regulating RA. Human RA fibroblast‐like synoviocyte (FLS) cell line MH7A cells was transfected by miR‐22 mimic and its control. CCK8 was utilized to detect cell proliferation. Cell apoptosis was analyzed by flow cytometry. MH7A cells stimulating with interleukin‐1β (IL‐1β) were transfected with miR‐22 mimic. Quantitative real time polymerase chain reaction (qRT‐PCR) and western blot assays were utilized to detect mRNA and protein expression. miR‐22 targets were predicted and validated by Targetscan and luciferase reporter assay. We revealed that miR‐22 showed downregulated expression in MH7A after stimulation with IL‐1β. Additionally, miR‐22 overexpression suppressed the proliferation and facilitated apoptosis in MH7A cells. IL6R was a target of miR‐22. Besides, miR‐22 overexpression inhibited the expression of IL6R and also suppressed inflammatory pathway NF‐κB. These results indicated that miR‐22 overexpression could restrain the activity of inflammation cells in RA by targeting IL6R and might be concerned with the inhibition of NF‐κB pathway.