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논문 기본 정보

자료유형
학술저널
저자정보
Dong-liang Shi (Henan Province Hospital of TCM) Gui-rong Shi (Shangqiu Medical College) Jing Xie (Henan Province Hospital of TCM) Xu-zhao Du (Henan Province Hospital of TCM) Hao Yang (Henan Province Hospital of TCM)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제39권 제8호
발행연도
2016.8
수록면
611 - 618 (8page)
DOI
molcells.2016.0103

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Fibroblast-like synoviocytes (FLS) with aberrant expres-sion of microRNA (miRNA) are critical pathogenic regula-tors in rheumatoid arthritis (RA). Previous studies have found that overexpression or silencing of miRNA can contribute to the development of miRNA-based therapeutics in arthritis models. In this study, we explored the effects of miR-27a on cell migration and invasion in cultured FLS from RA patients. We found that miR-27a was markedly downregulated in the serum, synovial tissue, and FLS of RA patients. Meanwhile, the expression of follistatin-like protein 1 (FSTL1) was upregulated, which suggests that FSTL1 plays a key role in RA development. The results of a Transwell assay showed that miR-27a inhibited FLS migration and invasion. However, miR-27a inhibition promoted the migration and invasion of FLS. In addition, the down-regulated expression of matrix metalloproteinases (MMP2, MMP9, and MMP13) and Rho family proteins (Rac1, Cdc42, and RhoA) was detected after treatment with miR-27a in RA-FLS by quantitative reverse transcription-PCR and western blot analysis. Then, a luciferase reporter assay validated that miR-27a targeted the 3-untranslated region (3?-UTR) of FSTL1. Moreover, miR-27a caused a significant decrease of FSTL1. In addition, the expression of TLR4 and NFκB was inhibited by miR-27a but increased by FSTL1 overexpression. In conclusion, we found that miR-27a inhibited cell migration and invasion of RA-FLS by targeting FSTL1 and restraining the TLR4/NFκB pathway.

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