UCA1 impacts progress of rheumatoid arthritis by inducing the apoptosis of fibroblast-like synoviocyte.

OBJECTIVE: Rheumatoid arthritis is a chronic autoimmune joint disease, which is characterized by the proliferation of fibroblast-like synoviocyte. Long non-coding RNA (lncRNA) has been reported to play an important role in the progression of many different diseases. The main objective of this research was to find out whether the lncRNAs influence the activity of fibroblast-like synoviocyte and the progression of this disease.

PATIENTS AND METHODS: qRT-PCR was used to detect the expression of UCA1 in fibroblast-like synoviocyte from normal people and rheumatoid arthritis patients. MTT assay was used to detect the viability of cells. Apoptosis was detected by Caspase-3 Colorimetric Activity Assay Kit (Millipore, Billerica, MA, USA). Western blot was used to analyze the relationship of UCA1 and apoptosis.

RESULTS: We found that the UCA1 was highly expressed in the normal fibroblast-like synoviocyte (NFLS), compared with the fibroblast-like synoviocyte of rheumatoid arthritis (RAFLS). We also found that the decrease in UCA1 expression increased the viability in NFLS and overexpressed UCA1 level in RAFLS decreased the viability. Caspase-3 was highly expressed in cells with higher viability. What's more, UCA1 could affect the viability of FLS by changing the expression of Wnt6.

CONCLUSIONS: According to the results, we found that UCA1 was closely related to rheumatoid arthritis, which could be a potential target for treating it.