Roles of bone morphogenetic protein binding endothelial regulator protein in obstructive hydronephrosis renal fibrosis of rats

Abstract

Objective To investigate the expression of bone morphogenetic protein binding endothelial regulator (BMPER) protein in the hydronephrotic kidney and its role in renal tissue fibrosis. Methods Thirty-six SPF male SD rats were randomly divided into acute obstruction group and sham operation group (n=18 each): irreducible complete unilateral ureteral obstruction (UUO) model or sham operation group model, respectively. On the postoperative week 1, 2, 4, 6, and 8, animals were killed, and the kidney tissue specimens were collected. Reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting were used to detect the expression of BMPER mRNA and protein in the hydronephrotic kidney tissues respectively. The BMPER lentiviral expression vector was constructed, and infected into human renal tubular epithelial HK-2 cells. The effect of BMPER protein on the transforming growth factor-β1 (TGF-β1)-induced HK-2 cell transdifferentiation, and the expression of α-smooth muscle actin (α-SMA) and Col-I protein during the transdifferentiation process were observed. Results The UUO model was successfully established. The expression of BMPER mRNA and protein was decreased gradually with the prolongation of obstruction time. High expression of BMPER protein could inhibit HK-2 cells transdifferentiation, and could significantly inhibit the expression of α-SMA and Col-I proteins during the transdifferentiation process (P<0.05). Conclusion The expression of BMPER in obstructive hydronephrosis in renal tissue is decreased. High expression of BMPER protein can inhibit renal tubular cell transdifferentiation, suggesting the anti-fibrosis effects of BMPER protein in obstructive hydronephrosis kidney tissues. Key words: Hydronephrotic kidney; Tissue fibrosis; Bone morphogenetic protein binding endothelial regulator protein