β1-Integrin is required for kidney collecting duct morphogenesis and maintenance of renal function

Wei Wu, Shinji Kitamura, David M. Truong, Timo Rieg, Volker Vallon, Hiroyuki Sakurai, Kevin T. Bush, David R. Vera, Robert S. Ross, Sanjay K. Nigam

Research output: Contribution to journalArticlepeer-review

Abstract

Deletion of integrin-β1 (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 altered growth and branching morphogenesis of the ureteric bud (the progenitor tissue of the renal collecting system), despite the apparent ability of the ureteric budderived 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.

Original languageEnglish (US)
Pages (from-to)F210-F217
JournalAmerican Journal of Physiology - Renal Physiology
Volume297
Issue number1
DOIs
StatePublished - Jul 2009

Keywords

  • Branching morphogenesis
  • Cystic kidney disease
  • Diabetes insipidus
  • Metanephric mesenchyme
  • Polyuria
  • Renal failure
  • Ureteric bud

ASJC Scopus subject areas

  • Physiology

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