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Objective@#To explore the effects of long non-coding RNA (LncRNA) MIR22HG on proliferation，apoptosis and inflammatory response of rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLSs) and its molecular mechanism．@*Methods@#Synovial tissue samples were collected from 37 RA patients and 30 joint trauma patients in our hospital，and the expression levels of MIR22HG and miR-22-5p in synovial tissue were detected by qRT-PCR. RA-FLSs in human was isolated ，cultured and identified in vitro． MIR22HG siRNA interference plasmid (si-MIR22HG) and its negative control plasmid (si-NC) ，miR-22-5p inhibitor and its negative control (inhibitorNC) were transfected into RA-FLSs respectively or simultaneously．The expression levels of MIR22HG and miR- 22-5p were detected by qRT-PCR. CCK-8 was used to detect the proliferation activity of cells in various groups. Annexin Ⅴ- FITC / PI was used to detect the apoptosis rates of cells in various groups．ELISA was used to detect the levels of TNF-α , IL-1 β and IL-6 in the supernatant of cells in various groups．Western blot was used to detect the protein expression levels of Bcl-2，Bax and Cleaved caspase-3 of cells in various groups．The targeting relationship between MIR22HG and miR-22-5p was verified by dual luciferase reporter gene assay. @*Results @#Compared with joint trauma patients，the expression level of MIR22HG in synovial tissues of RA patients increased (P＜0. 05) ， while the expression level of miR-22-5p decreased (P＜0. 05) ．Interference with MIR22HG inhibited the proliferation activity of RA-FLSs，decreased the levels of TNF-α , IL-1 β and IL-6 in cell supernatant and the protein expression level of Bcl-2 in cells (P＜0. 05) ，and increased the apoptosis rate，the expression level of miR-22-5p and the protein expression levels of Bax and Cleaved casepase-3 (P ＜0. 05 ) ．However，inhibition of miR-22-5p expression reversed the effects of MIR22HG gene silencing on proliferation，apoptosis and inflammation of RA-FLSs (P＜0. 05) ．Dual luciferase reporting assay showed that miR-22-5p was a potential downstream miRNA target of MIR22HG．@*Conclusion@# MIR22HG is highly expressed in synovial tissues of RA patients，and it may promote the proliferation and the inflammatory response of RA-FLSs and inhibit cell apoptosis by down regulating the expression of miR-22-5p.
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PURPOSE: Tubulointerstitial hypoxia in the kidney is considered a hallmark of injury and a mediator of the progression of tubulointerstitial fibrosis. Hypoxia-inducible factor-1alpha (HIF-1alpha), a master transcription factor in cellular adaptation to hypoxia, regulates a wide variety of genes, some of which are closely associated with tissue fibrosis. The present study set out to characterize urinary HIF-1alpha expressions in patients with lupus nephritis (LN) and to explore whether urinary HIF-1alpha expressions are associated with histologic chronicity changes and renal function. MATERIALS AND METHODS: Urinary HIF-1alpha levels were measured by enzyme-linked immunosorbent assays in 42 patients with LN and in 30 healthy controls. Activity and chronicity indexes as well as tubular HIF-1alpha expressions were analyzed for each specimen. RESULTS: Urinary HIF-1alpha levels were higher in LN patients than in healthy controls (3.977+/-1.696 vs. 2.153+/-0.554 ng/mL, p0.05). CONCLUSION: Urinary HIF-1alpha levels were elevated in LN patients and were associated with histologic chronicity changes and renal function, indicating that HIF-1alpha might contribute to histologic chronicity in LN.