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Originally published In Press as doi:10.1074/jbc.M204806200 on May 30, 2002

J. Biol. Chem., Vol. 277, Issue 34, 31154-31162, August 23, 2002
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Determinants of Vascular Permeability in the Kidney Glomerulus*

Yuki HamanoDagger , James A. GrunkemeyerDagger , Akulapalli SudhakarDagger , Michael ZeisbergDagger , Dominic Cosgrove§, Roy Morello, Brendan Lee, Hikaru SugimotoDagger , and Raghu KalluriDagger ||

From the Dagger  Program in Matrix Biology, Divisions of Gastroenterology and Nephrology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, § Gene Expression Laboratory, Boystown National Research Hospital, Omaha 68131, Nebraska, and  Department of Molecular and Human Genetics, Baylor College of Medicine, Houston 77030, Texas

The human kidneys filter 70 liters of blood plasma every day. The hallmark of almost all kidney diseases, whether acquired or genetic, is the leakage of plasma proteins into the urine because of alterations in the glomerular filtration unit of the kidney. In this regard, the human mutations in nephrin, podocin, alpha -actinin-4, COL4A3, and COL4A5 genes expressed in the glomeruli have been implicated to cause alterations in glomerular filtration apparatus. Nevertheless, the expression of these proteins in relation to each other in mouse models for glomerular vascular leak is unknown. Additionally, within the glomerulus, the central question of whether the primary filtration barrier is the basement membrane or the epithelial slit diaphragm remains ambiguous. Therefore, in this study, we examined the localization and expression of glomerular epithelial slit diaphragm and glomerular basement membrane proteins implicated in glomerular vascular leak using mice deficient in either the alpha 3 chain of type IV collagen, the major constituent of glomerular basement membrane, or LMX1B transcription factor, which regulates the expression of key glomerular type IV collagen genes COL4A3 and COL4A4 or nephrin, a glomerular epithelial slit diaphragm-associated protein. This study demonstrates that decreased expression of slit diaphragm protein, nephrin, correlates with a loss of glomerular filter integrity. Additionally, we demonstrate that defects induced by proteins of glomerular basement membrane lead to an insidious plasma protein leak, whereas the defects induced by proteins in the glomerular epithelial slit diaphragms lead to a precipitous plasma protein leak.

* This work was supported in part by Grants DK 51711 and DK 55001 from the National Institutes of Health, the Program in Matrix Biology at the BIDMC, Japan Research Foundation for Clinical Pharmacology (to Y. H.), and National Research Service Award Grant DK 09946 from the National Institutes of Health (to J. A. G.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AF191090 and AF190638.

|| To whom correspondence should be addressed: Dept. of Medicine, Harvard Medical School, Program in Matrix Biology, DANA 514, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215. Tel.: 617-667-0445; Fax: 617-975-5663; E-mail: rkalluri@caregroup.harvard.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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