#3428 DEPLETED HDAC3 ATTENUATES HYPERURICEMIA-INDUCED RENAL INTERSTITIAL FIBROSIS VIA MIR-19B-3P/SF3B3 AXIS

Abstract Background and Aims Hyperuricemia (HN) is a threat for the occurrence of renal interstitial fibrosis (RIF). Dysfunctional histone deacetylase 3 (HDAC3) elicit damage. This study aimed to explore role HDAC3 in HN-induced RIF from microRNA-19b-3p/splicing factor 3b subunit (miR-19b-3p/SF3B3) axis. Method 1. The HN model was established on rats induce by oral administration adenine potassium oxalate; 2. were injected with related vectors (sh-HDAC3, mimic-miR-19b-3p, sh-HDAC3+miR-19b-3p inhibitor) suppress and/or promote miR-19b-3p; detection indicators are listed as follows: (1) Blood samples urine collected UA, BUN, Scr 24 h protein measurement; (2) Renal pathological damages, index cell apoptosis measured HE, Masson TUNEL staining; (3) α-SMA, TGF-β1 FN contents tissues detected IHC (4) mRNA levels HDAC3, miR-19b-3p SF3B3 RT-qPCR WB. (5) Interaction ChIP dual luciferase reporter gene assay; (6) predicted/detected bioinformatics website/dual assay. Results induced dysfunction, rats; showed elevated reduced tissues. Suppressed or promoted relieved apoptosis; bound promoter negatively regulated SF3B3; depletion abrogated down-regulated HDAC3-induced effects RIF. Conclusion regulate SF3B3. Depressed relived restoring knocking down Targeting miR-19b-3p/SF3B3 axis may be promising therapeutic strategy preventing