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Am J Physiol Renal Physiol (May 13, 2009). doi:10.1152/ajprenal.90260.2008
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Submitted on April 18, 2008
Revised on April 9, 2009
Accepted on May 8, 2009

{beta}1 INTEGRIN IS REQIRED FOR KIDNEY COLLECTING DUCT MORPHOGENESIS AND MAINTENANCE OF RENAL FUNCTION

Wei Wu1, Shinji Kitamura, David M Truong, Timo Rieg2, Volker Vallon3, Hiroyuki Sakurai4, Kevin T. Bush1, David Vera, Robert Scott Ross5, and Sanjay K. Nigam1*

1 University of California, San Diego
2 UCSD
3 University of California San Diego & VAMS
4 University of California San Diego
5 UCSD School of Medicine and Veterans Administration Healthcare San Diego

* To whom correspondence should be addressed. E-mail: snigam{at}ucsd.edu.

Deletion of Integrin {beta}1 (Itgb1) in the kidney collecting system led to progressive renal dysfunction and polyuria. The defect in the concentrating ability of the kidney was concomitant with decreased medullary collecting duct expression of aquaporin 2 and arginine-vasopressin receptor 2, while histological examination revealed hypoplastic renal medullary collecting ducts characterized by increased apoptosis ectasia and cyst formation. In addition, a range of defects from small kidneys with cysts and dilated tubules to bilateral renal agenesis was observed. This was likely due to reduced growth and branching of the ureteric bud (the progenitor tissue of the renal collecting system), despite the apparent ability of the UB-derived cells to induce differentiation of the metanephric mesenchyme. These data not only support a role for Itgb1 in the development of the renal collecting system, but also raise the possibility that Itgb1 links morphogenesis to terminal differentiation and ultimately collecting duct function and/or maintenance.




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