#5526 COMPLEMENT C3 EXERTS DIRECT PRO-FIBROTIC EFFECTS ON KIDNEY TUBULES

Abstract Background and Aims Renal complement expression has been observed in both experimental human kidney diseases. We have previously reported massive tubular C3 fibrotic TGF-beta1 transgenic mice (Nephrol Dial Transpl 2015, 30; S3:FP301). Still, little is known whether this intra-renal only an inflammatory marker of renal fibrosis or also exerts direct pro-fibrotic effects the pathogenesis. In present study we aimed to investigate effect C3a receptor activation murine primary epithelial cells. Method Primary cells (TEC) were isolated from kidneys four weeks-old male C57Bl6 mouse. The grown DMEM/12 medium supplemented with 2% FBS recombinant 5 ng/ml EGF, characterized for mesenchymal markers. Verified TEC between P4 P10 passages used experiments. seeded on 6-well plates treated 24 hours PBS (CTL, n=3), 100 nM agonist peptide (C3aR, n=3) 10 (TGFb, n=3). Then, mRNA protein expressions assessed evaluated using Kruskal-Wallis test (p<0.05). Results TGF-beta induced a 2-fold Col1a1 1,6-fold Tgfb1 expression, accompanied by 4-fold Egr2 but did not affect Ccl2 expression. contrast, C3aR group depicted 1,8-fold 1,5-fold Despite similar overexpression TGFb groups, marked TGFB1 (15-fold) was group. Conclusion Our data indicate that production can exert autocrine / paracrine unrelated levels. Therefore, local might play significant pathogenetic role fibrosis.