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1 Renal Division, Department of Internal Medicine, and 3 Center for Immunology and Department of Pathology, Washington University School of Medicine, St. Louis, Missouri 63110; and 2 Biocenter and Department of Biochemistry, University of Oulu, 90570 Oulu, Finland
CD2-associated
protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic
domain of nephrin, a component of the glomerular slit diaphragm. Mice
lacking CD2AP exhibit a congenital nephrotic syndrome characterized by
extensive foot process effacement, suggesting that CD2AP-nephrin
interactions are critical to maintaining slit diaphragm function. We
have examined the patterns of expression of both CD2AP and nephrin in
developing mouse and human kidney. Both proteins were first detected in
developing podocytes at the capillary loop stage of glomerulogenesis
and eventually became concentrated near the glomerular basement
membrane. CD2AP was also observed diffusely in collecting duct and
apically in many cells of proximal and distal tubule. Kidneys from
Cd2ap 
/ mice initially exhibited normal nephrin
localization, but as the mice aged and foot processes became effaced,
nephrin disappeared. In laminin-
2 mutant mice exhibiting
nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a
primarily punctate pattern. Extensive extrarenal expression of CD2AP
was observed in endothelial and epithelial cells, in many cases with a
specific subcellular localization. Together, these results suggest that
CD2AP is not only involved in maintaining the slit diaphragm but
may also have a general role in maintaining specialized subcellular
architecture. The severity of kidney disease in Cd2ap mutant
mice may have eclipsed manifestation of defects in other tissues.
CD2-associated protein; renal development; nephrotic syndrome; glomerulus; nephron; epithelia
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