Prostatic ductal system in rats: Changes in regional distribution of extracellular matrix proteins during castration-induced regression

BACKGROUND. The extracellular matrix (ECM) is an intricate network composed of an array of molecules that play an integral role in the regulation of c ell function, differentiation, and tissue-specific gene expression in vario us epithelia. In the present study, we examined the distribution of collage n type TV and laminin along the rat ventral prostatic duct before and after castration. METHODS. Mature Sprague-Dawley rats were castrated and their prostates proc essed for immunocytochemistry of ECM proteins, laminin, and collagen type I V. Tissue sections were also processed for apoptosis staining, using the 3' end-labeling technique. To examine the effect of ECM proteins on epithelia l growth, rat ventral epithelial cells were cultured on ECM-coated surfaces . RESULTS. In the intact rat, laminin was localized in the basement membrane along all regions of the ventral prostate ductal system. Collagen type TV w as found to be distributed evenly in the basement membrane of the distal an d intermediate regions but was absent or poorly organized in the proximal r egion, where apoptosis in the epithelium occurs at a high rate. In the regr essing prostate after castration, there was a shift in apoptosis from the p roximal region to the distal intermediate regions of the prostatic duet. As sociated with the shift was a remodeling of basement membrane proteins due to the specific loss of collagen type IV in the distal and intermediate reg ions. Collagen type IV reappeared underneath the epithelium 7 days after ca stration, when apoptosis in the epithelium stopped. In vitro, collagen type IV enhanced the growth of ventral prostatic epithelial cells, as assessed by cell number. CONCLUSIONS. Collagen basement membrane type IV mediates growth of rat vent ral prostate epithelium, and its loss during tissue remodeling after castra tion is associated with cell death. Prostate 43:3-10, 2000. (C) 2000 Wiley- Liss, Inc.