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Background: Epithelial cells of the rat coagulating gland secrete a minor fraction of proteins by means of an alternative export mode named apocrine secretion. Thereby, proteins are released by means of membrane bounded blebs or "aposomes" arising from the apical plasma membrane. Little is known about the composition of the aposomal membrane and whether or not proteins located in the apical plasma membrane are integrated into the aposomes., Methods: To show expression and localization of Ca(2+)-ATPase in rat coagulating gland, reverse transcriptase-polymerase chain reaction, Western blotting experiments, and Ca(2+)-ATPase activity assays, as well as immunofluorescence studies were performed., Results: Ca(2+)-ATPase is located in the apical plasma membrane of the epithelial cells of the rat coagulating gland and is also included in the aposomes. Mg(2+)-dependent and Mg(2+)-independent Ca(2+)-ATPase activity was observed in coagulating gland primary epithelial cells and tissue. Gene expression of plasma membrane Ca(2+)-ATPase isoforms 1 and 4 was detected in cultured primary epithelial cells of the rat coagulating gland and coagulating gland tissue., Conclusions: We show for the first time that Ca(2+)-ATPase as an important, functionally active membrane protein of the apical plasma membrane is incorporated into the aposomal membranes and is released from the cells during apocrine secretion process., (Copyright 2002 Wiley-Liss, Inc.)

Prostatic smooth muscle cells have been regarded to play a major pathogenetic role during the development of benign prostatic hyperplasia (BPH) in elderly men. Altered hormonal signals (increased estrogen) have been made responsible for the "metabolic" transformation of prostatic smooth muscle cells, which were thought to produce increased amounts of connective tissue fibers observed in BPH. In order to find out the role of metabolically "activated" smooth muscle cells, hormone stimulation experiments were performed in male rats. The effects of androgen deprivation and estrogen stimulation were recorded by semiquantitative analysis of intermediate and myofilament proteins in stromal smooth muscle cells. In castrated or estrogen-treated or estrogen-treated and castrated animals, the reduction of the glandular lumen is the most obvious morphological alteration, accompanied by an increase in connective tissue. Regressive changes occurred most rapidly in castrated animals (already within the first week), slower in castrated estrogen-treated animals and still slower in normal estrogen-treated animals. Regression of the epithelium was accompanied by a marked decrease in immunoreactivity for prostatic binding protein (PBP) in castrated animals, while PBP immunoreactivity in estrogenized animals was retained for up to 6 weeks. Smooth muscle cells became atrophic in castrated animals. This effect was attenuated in estrogen-treated animals. There was no indication for enhanced collagen synthesis by smooth muscle cells. Actin and desmin-immunoreactivity were only slightly altered in experimental animals and showed a changed distribution pattern. Prostatic smooth muscle cells respond less markedly to hormonal alterations than do the fibroblasts.

Fine structural alterations of the canine prostate induced by long-term treatment of castrated adult animals with estrogens and/or androgens and also in combination with antiandrogens and/or antiestrogens for six months have been studied with particular respect to their topographic location within the gland. Three major patterns of structural responses of the epithelium have been distinguished: squamous metaplasia, atrophy, and hypertrophy, while in stroma, regression, hypertrophy, or sclerosis were observed. In addition to cellular alterations of stromal fibrocytes and smooth muscle cells, characteristic changes in the arrangement, distribution, and pattern of the different stromal elements occurred. General squamous metaplasia of the epithelium and regressive alterations of stromal cells were most obvious in animals treated with estradiol plus androstanediol. Atrophy of the epithelium and stromal sclerosis were the salient features of antiandrogen-treated castrated animals, while hypertrophy or hyperplasia of both the epithelium and stroma was a major finding in androstanediol-substituted castrated animals. Combined treatment caused rather heterogeneous structural patterns seemingly dependent on the location within the gland. The results indicate that the prostatic epithelial cells dispose of a broad variety of structural reaction patterns that, in case of combined hormonal treatment, are expressed in a manner typical for their locations within the ductal system of the gland. However, with the exception of combined treatment with estradiol, tamoxifen, and androstanediol of castrated dogs, none of the experimental protocols used induced a morphologic response of the gland comparable to that seen in human benign prostatic hyperplasia. The canine prostate therefore is of rather limited value as a model for human BPH.