Severe fibronectin-deposit renal glomerular disease in mice lacking uteroglobin

Zhongjian Zhang, Gopal C. Kundu, Chiun-Jye Yuan, Jerrold M. Ward, Eric J. Lee, Francesco DeMayo, Heiner Westphal, Anil B. Mukherjee*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

109 Scopus citations

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.

Original languageEnglish
Pages (from-to)1408-1412
Number of pages5
JournalScience
Volume276
Issue number5317
DOIs
StatePublished - 30 May 1997

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