LOSS OF THE BASEMENT-MEMBRANE MATRIX MOLECULE, BAMIN, IN DIPHENYLAMINE-TREATED MICE

Polycystic kidney disease (PKD) is a life-threatening disease characte rized by focal dilatations or cysts in certain kidney tubules. Changes (i. e. thickening) in the support structure for these tubules, the ba sement membrane, have been related to the development of the cysts. An alysis of changes in basement membranes of humans with PKD is difficul t, however, due to the restricted amount of material available for stu dy. Several genetic and induced animal models, including diphenylamine -treated rats, have been employed to study the effects of PKD on basem ent membrane synthesis. While all these studies agree that PKD has a s ignificant influence on basement membranes, no clear understanding as to how PKD effects basement membrane composition has emerged. Here, we report our findings of the effect of diphenylamine treatment on the c omposition of the basement membrane. Our immunohistological studies in dicate that bamin, a recently described glycoprotein associated with g lomerular basement membranes (Robinson et al., 1989), is not present i n the glomerular basement membranes of diphenylamine-treated mice. Thi s finding was confirmed by analysis of the composition of the basement membrane matrix synthesized by EHS tumors grown in control and diphen ylamine-treated mice. The possible role of bamin in the pathogenesis o f renal cysts is discussed.