Report

Severe Fibronectin-Deposit Renal Glomerular Disease in Mice Lacking Uteroglobin

See allHide authors and affiliations

Science  30 May 1997:
Vol. 276, Issue 5317, pp. 1408-1412
DOI: 10.1126/science.276.5317.1408

You are currently viewing the abstract.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Abstract

Despite myriads of biological activities ascribed to uteroglobin (UG), a steroid-inducible secreted protein, its physiological functions are unknown. Mice in which the uteroglobin gene was disrupted had severe renal disease that was associated with massive glomerular deposition of predominantly multimeric fibronectin (Fn). The molecular mechanism that normally prevents Fn deposition appears to involve high-affinity binding of UG with Fn to form Fn-UG heteromers that counteract Fn self-aggregation, which is required for abnormal tissue deposition. Thus, UG is essential for maintaining normal renal function in mice, which raises the possibility that an analogous pathogenic mechanism may underlie genetic Fn-deposit human glomerular disease.

  • * To whom correspondence should be addressed: E-mail: mukherja{at}cc1.nichd.nih.gov

View Full Text