BACKGROUND: Extracellular matrix accumulation, epithelial-to-mesenchymal transition, tubular atrophy and loss of peritubular capillary network are hallmarks of tubulointerstitial injury in progressive renal diseases. In this study, we analyzed endostatin expression in kidneys subjected to unilateral ureteral obstruction (UUO). METHODS: Collagen XVIII mRNA expression was evaluated by real-time polymerase chain reaction (PCR). Endostatin and CD31 protein levels were analyzed by Western blot and immunohistochemistry. In vitro quantification of collagen XVIII and fibrosis-related genes in HK2 cells was performed by real-time PCR. RESULTS: UUO significantly increased collagen XVIII mRNA expression and released a 30-kDa endostatin fragment. Immunohistochemistry revealed endostatin expression increased in injured tissue, mainly on tubular cells. Of interest, expression of CD31 was significantly reduced by UUO. Endostatin administration in vitro did not modify the expression of genes related to fibrosis development. However, in vitro TGF-beta1 administration induced expression of collagen XVIII/endostatin mRNA in human tubular cells. CONCLUSION: Endostatin is expressed during the progression of renal fibrosis in vitro and in vivo, suggesting a role for endostatin in development of tubulointerstitial injury.
BACKGROUND: Extracellular matrix accumulation, epithelial-to-mesenchymal transition, tubular atrophy and loss of peritubular capillary network are hallmarks of tubulointerstitial injury in progressive renal diseases. In this study, we analyzed endostatin expression in kidneys subjected to unilateral ureteral obstruction (UUO). METHODS:Collagen XVIII mRNA expression was evaluated by real-time polymerase chain reaction (PCR). Endostatin and CD31 protein levels were analyzed by Western blot and immunohistochemistry. In vitro quantification of collagen XVIII and fibrosis-related genes in HK2 cells was performed by real-time PCR. RESULTS: UUO significantly increased collagen XVIII mRNA expression and released a 30-kDa endostatin fragment. Immunohistochemistry revealed endostatin expression increased in injured tissue, mainly on tubular cells. Of interest, expression of CD31 was significantly reduced by UUO. Endostatin administration in vitro did not modify the expression of genes related to fibrosis development. However, in vitro TGF-beta1 administration induced expression of collagen XVIII/endostatin mRNA in human tubular cells. CONCLUSION:Endostatin is expressed during the progression of renal fibrosis in vitro and in vivo, suggesting a role for endostatin in development of tubulointerstitial injury.
Authors: Heleen Rienstra; Kirankumar Katta; Johanna W A M Celie; Harry van Goor; Gerjan Navis; Jacob van den Born; Jan-Luuk Hillebrands Journal: PLoS One Date: 2010-02-05 Impact factor: 3.240
Authors: Jacqueline Wallwitz; Petra Aigner; Elisabeth Gadermaier; Eva Bauer; Emilio Casanova; Anton Bauer; Dagmar Stoiber Journal: PLoS One Date: 2019-08-12 Impact factor: 3.240
Authors: Juliane Merl-Pham; Trayambak Basak; Larissa Knüppel; Deepak Ramanujam; Mark Athanason; Jürgen Behr; Stefan Engelhardt; Oliver Eickelberg; Stefanie M Hauck; Roberto Vanacore; Claudia A Staab-Weijnitz Journal: Matrix Biol Plus Date: 2019-04-13
Authors: Rui Z Bai; Yang Wu; Quan Liu; Ke Xie; Yu Q Wei; Yong S Wang; Kang Liu; Yan Luo; Jing M Su; Bing Hu; Ji Y Liu; Qiu Li; Ting Niu; Zhi W Zhao; Li Yang Journal: J Exp Clin Cancer Res Date: 2009-03-05