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• W1972528145 abstract "No AccessJournal of UrologyTestis, Varicocele and Stones1 May 2015Cell Type Specific Changes in BMP-7 Expression Contribute to the Progression of Kidney Disease in Patients with Obstructive Uropathy Scott R. Manson, Joseph B. Song, Qiusha Guo, Helen Liapis, and Paul F. Austin Scott R. MansonScott R. Manson Equal study contribution. More articles by this author , Joseph B. SongJoseph B. Song Equal study contribution. More articles by this author , Qiusha GuoQiusha Guo More articles by this author , Helen LiapisHelen Liapis More articles by this author , and Paul F. AustinPaul F. Austin Financial interest and/or other relationship with the Food and Drug Administration, and Allergan. More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.10.117AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: Congenital urinary tract obstruction is a leading cause of renal maldevelopment and pediatric kidney disease. Nonetheless, few groups have examined its molecular pathogenesis in humans. We evaluated the role of BMP-7, a protein required for renal injury repair and nephrogenesis, in disease progression in patients with obstructive uropathy. Materials and Methods: Whole kidney and cell specific BMP-7 expression was examined in a murine model of unilateral ureteral obstruction and in patients with congenital ureteropelvic junction obstruction. Findings were correlated with molecular markers of renal injury and clinical parameters. Results: Unilateral ureteral obstruction led to a dramatic decrease in BMP-7 expression in the proximal and distal tubules before the onset of significant loss of renal architecture and fibrosis, suggesting that this is a critical molecular event that drives early stage disease progression. Loss of BMP-7 expression then extended to the collecting ducts and glomeruli in end stage kidney disease. When translating these findings to patients with ureteropelvic junction obstruction, global loss of BMP-7 expression correlated with a decreased number of nephrons, loss of renal architecture, severe renal fibrosis and loss of kidney function. Conclusions: Given that BMP-7 has a critical role in renal injury repair and nephrogenesis, these findings show that cell specific changes in BMP-7 expression contribute to the onset of irreversible renal injury and impaired kidney development secondary to congenital urinary tract obstruction. Accordingly therapies that target these cell populations to restore BMP-7 activity may limit disease progression in patients with obstructive uropathy. References 1 : Obstructive uropathy: an important cause of chronic renal failure in children. Clin Pediatr (Phila)2002; 41: 309. Google Scholar 2 : Renal abnormalities and their developmental origin. Nat Rev Genet2007; 8: 791. Google Scholar 3 : Obstructive uropathy. Early Hum Dev2006; 82: 15. Google Scholar 4 : Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy. Pediatr Nephrol2010; 25: 687. Google Scholar 5 : The kidney in congenital ureteropelvic junction obstruction: a spectrum from normal to nephrectomy. J Urol2008; 179: 1257. Link, Google Scholar 6 : The BMP-7-Smad1/5/8 pathway promotes kidney repair after obstruction induced renal injury. J Urol2011; 185: 2523. Link, Google Scholar 7 : Endogenous BMP-7 is a critical molecular determinant of the reversibility of obstruction-induced renal injuries. Am J Physiol Renal Physiol2011; 301: F1293. Google Scholar 8 : BMP-7 counteracts TGF-beta1-induced epithelial-to-mesenchymal transition and reverses chronic renal injury. Nat Med2003; 9: 964. Google Scholar 9 : Bone morphogenic protein-7 induces mesenchymal to epithelial transition in adult renal fibroblasts and facilitates regeneration of injured kidney. J Biol Chem2005; 280: 8094. Google Scholar 10 : Bone morphogenic protein-7 inhibits progression of chronic renal fibrosis associated with two genetic mouse models. Am J Physiol Renal Physiol2003; 285: F1060. Google Scholar 11 : Osteogenic protein-1 prevents renal fibrogenesis associated with ureteral obstruction. Am J Physiol Renal Physiol2000; 279: F130. Google Scholar 12 : Renal bone morphogenetic protein-7 protects against diabetic nephropathy. J Am Soc Nephrol2006; 17: 2504. Google Scholar 13 : Bone morphogenetic protein-7 improves renal fibrosis and accelerates the return of renal function. J Am Soc Nephrol2002; 13: S14. Google Scholar 14 : Bone morphogenic protein-7 (BMP-7), a novel therapy for diabetic nephropathy. Kidney Int2003; 63: 2037. Google Scholar 15 : Osteogenic protein-1 (bone morphogenetic protein-7) reduces severity of injury after ischemic acute renal failure in rat. J Clin Invest1998; 102: 202. Google Scholar 16 : Localized expression of human BMP-7 by BM-MSCs enhances renal repair in an in vivo model of ischemia-reperfusion injury. Genes Cells2012; 17: 53. Google Scholar 17 : Role of the TGF-beta/BMP-7/Smad pathways in renal diseases. Clin Sci (Lond)2013; 124: 243. Google Scholar 18 : Divergence and convergence of TGF-beta/BMP signaling. J Cell Physiol2001; 187: 265. Google Scholar 19 : TGF-beta in renal injury and disease. Semin Nephrol2007; 27: 309. Google Scholar 20 : A requirement for bone morphogenetic protein-7 during development of the mammalian kidney and eye. Genes Dev1995; 9: 2795. Google Scholar 21 : BMP-7 is an inducer of nephrogenesis, and is also required for eye development and skeletal patterning. Genes Dev1995; 9: 2808. Google Scholar 22 : Podocyte-derived BMP7 is critical for nephron development. J Am Soc Nephrol2008; 19: 2181. Google Scholar 23 : Renal structural and functional repair in a mouse model of reversal of ureteral obstruction. J Am Soc Nephrol2005; 16: 3623. Google Scholar 24 : Aquaporin-1 water channel expression in human kidney. J Am Soc Nephrol1997; 8: 1. Google Scholar 25 : Localization of Tamm-Horsfall glycoprotein in the human kidney using immuno-fluorescence and immuno-electron microscopical techniques. J Anat1981; 132: 597. Google Scholar 26 : Expression of AQP family in rat kidneys during development and maturation. Am J Physiol1997; 272: F198. Google Scholar 27 : Dedifferentiation and proliferation of surviving epithelial cells in acute renal failure. J Am Soc Nephrol2003; 14: S55. Google Scholar 28 : Epithelial-mesenchymal-epithelial cycling in kidney repair. Curr Opin Nephrol Hypertens2008; 17: 379. Google Scholar 29 : Loss of tubular bone morphogenetic protein-7 in diabetic nephropathy. J Am Soc Nephrol2001; 12: 2392. Google Scholar 30 : The Society for Fetal Urology consensus statement on the evaluation and management of antenatal hydronephrosis. J Pediatr Urol2010; 6: 212. Google Scholar © 2015 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 193Issue 5SMay 2015Page: 1860-1869 Advertisement Copyright & Permissions© 2015 by American Urological Association Education and Research, Inc.Keywordsbone morphogenetic protein 7kidneyfibrosisureteral obstructiongrowth and developmentMetricsAuthor Information Scott R. Manson Equal study contribution. More articles by this author Joseph B. Song Equal study contribution. More articles by this author Qiusha Guo More articles by this author Helen Liapis More articles by this author Paul F. Austin Financial interest and/or other relationship with the Food and Drug Administration, and Allergan. More articles by this author Expand All Advertisement PDF downloadLoading ..." @default.
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• W1972528145 title "Cell Type Specific Changes in BMP-7 Expression Contribute to the Progression of Kidney Disease in Patients with Obstructive Uropathy" @default.
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• W1972528145 cites W2114245705 @default.
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• W1972528145 cites W2117676407 @default.
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