Effects of castration and androgens upon prostatic proteoglycans in rats

Kofoed, J. A.; Tumilasci, Omar R.; Curbelo, H.M.; Lemos, S M Fernández; Arias, Nieves; Houssay, Alberto B.

doi:10.1002/pros.2990160202

Cited by 21 publications

(17 citation statements)

References 7 publications

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“…There is also evidence that one or more serine proteases may be required, either to activate the enzyme proteolytically or to initiate the degradation of the nuclear matrii, to render the DNA more accessible to the endonucleases. Analysis of the fragments has shown that DNA fragmentation is probably a stepwise process, involving fragmentation at interrosette sites (generating DNA fragments larger than 300 kb), interloop sites (generating fragments of about 50 The secretory epithelial cells of the prostate interact with the basement membrane located between the stroma and the epithelium. Several lines of evidence suggest that the normal function of secretory epithelial cells is dependent on a complex interplay between the epithelium, the ECM and the underlying mesenchyme or stroma [2 51.…”

Section: Dna Fragmentationmentioning

confidence: 99%

Apoptosis, tumour invasion and prostate cancer

Tenniswood

1997

British Journal of Urology

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IntroductionCell death, or apoptosis, is not a single phenomenon but a series of morphologically and biochemically related processes [1,2]. Cell death of lymphocytes and other cells of reticulo-endothelial origin is dominated by changes in nuclear morphology [3], while apoptotic death of glandular epithelial cells, such as those of the prostate, requires profound cytoplasmic changes and alterations in the cell-cell and cell-substratum interactions [4]. The rodent prostate is a very useful model for the study of apoptosis induced by hormone withdrawal, The gland is an arborhed network of ducts, with several cell types that display anatomical and biochemical heterogeneity and substantially different sensitivities to androgen ablation. nor the basal cells that are also localized to the proximal region, appear to require androgens for survival. The prostate begins to regress about 12 h after castration, when the level of Sct-DHT falls below that needed to inhibit involution [lo]. The reduction in prostate size that occurs over the next 3-6 days is primarily due to the selective loss of the secretory luminal epithelial cells in the distal and intermediate regions, resulting in the complete obliteration of many of the ducts while maintaining the proximal segments of the ducts after castration. The process of apoptosis in the prostate can be broken down into several stages (Fig. 1). During the precondensation stage, many of the genes that are necessary for cell death are induced de now, or recruited from other functions in the gland. The length of the precondensation stage appears to vary from cell to cell and probably reflects the microheterogeneity in the hormone or growth factor environment. The precondensation phase is followed by cytoplasmic condensation which involves the loss of the interactions between the dying cell and its neighbours as the extra-cellular matrix (ECM) is degraded and the cytoplasmic volume decreases. During nuclear condensation, the activation of one or more endonucleases results in the fragmentation of the DNA and its marginalization to the nuclear periphery, Producing the hyperchromatic, pyknotic nucleus characteristic of apoptotic cells. As the initiation of apoptosis in glandular tissues is stochastic, it is difficult to separate clearly cytoplasmic and nuclear condensation temporally in vivo, but in isolated cells from other tissues (e.g. granulosal cells), nuclear condensation is clearly initiated after cytoplasmic condensation. During the fragmentation phase the apoptotic cell is subdivided into several apoptotic bodies which are subsequently phagocytosed by the neighbouring epithelial cells or macrophages and degraded by the lysosomal enzymes, activated either in the host cell or in the apoptotic body [l 11. Remarkably, this latter process occurs with no leakage of the intracelMar components into the extracellular space, ensuring that the complement cascade system is not activated and that there is no inflammatory response. This feature distinguishes apoptosis from necrosis. In the pr...

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Section: Dna Fragmentationmentioning

confidence: 99%

Apoptosis, tumour invasion and prostate cancer

Tenniswood

1997

British Journal of Urology

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“…The secretory cells of the prostate interact with the basement membrane located between the stroma and epithelium. The extracellular matrix contains a number of components including fibronectin, collagen, laminin, vitronectin, heparan sulfate, and chondroitin sulfate (Kofoed et al 1990;Paulsson 1992). These components are known to interact with their cognate receptors, many of which are members of the integrin superfamily (Hynes 1992;Damsky and Werb 1992;Juliano and Haskil 1993).…”

Section: Role Of the Extracellular Matrix Proteases And Growthmentioning

confidence: 99%

The role of growth factors in the suppression of active cell death in the prostate: an hypothesis

Guenette¹,

Tenniswood²

1994

Biochem. Cell Biol.

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Regression of the rat ventral prostate occurs when the level of 5 alpha-dihydrotestosterone, the trophic hormone, drops below the threshold required to suppress apoptosis. The induction of apoptosis in the ventral prostate is accompanied by the increase in the steady-state level of a number of mRNAs coding for proteins that are involved in the latter stages of apoptosis and thus represent secondary thanatogens. These include proteases (cathepsins, plasminogen activators, and collagenase), clusterin, poly(ADP)ribose polymerase, tenascin, and several unidentified genes, as well as several RNases and the classical Ca2+,Mg(2+)-dependent endonuclease. In addition, insulin-like growth-factor-binding protein 5 (IGFBP-5) is induced de novo. We propose that IGFBP-5 may serve to trigger the apoptotic process through the attenuation of the insulin-like growth factor signalling system (which is necessary for cell survival), and as such, represents a primary thanatogen in the prostate.

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“…The prostatic stroma is rich in extracellular matrix (ECM) elements such as collagen Wbers (Vilamaior et al 2000), proteoglycans (Kofoed et al 1990), laminin (Carvalho and Line 1996), Wbronectin and elastin (Carvalho et al 1997). In addition to a structural role, the ECM and related molecules have been recognized as key regulatory components during developmental morphogenesis and cell diVerentiation of many branched organs (Timpl 1989;Gilbert 2006).…”

Section: Introductionmentioning

confidence: 98%

Localized matrix metalloproteinase (MMP)-2 and MMP-9 activity in the rat ventral prostate during the first week of postnatal development

Bruni‐Cardoso

Vilamaior

Taboga

et al. 2008

Histochem Cell Biol

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The initial events in prostatic morphogenesis involve cell proliferation, epithelial canalization and outgrowth toward the stroma. We have hypothesized that stromal rearrangement takes place at the sites of epithelial growth and branching and that this rearrangement involves the action of gelatinases matrix metalloproteinase (MMP)-2 and MMP-9. Thus, the purpose of the present study was to characterize structural aspects of epithelial growth during the first week of postnatal development of the rat ventral prostate and to investigate the expression, localization and activity of MMP-2 and MMP-9 during this period by histological, ultrastructural and immunocytochemical analysis, in addition to gel zymography, in situ zymography and Western blotting. An increasing complexity of prostatic architecture was observed within the first postnatal week. Concurrently, the stroma became more organized and some cells differentiated into smooth muscle cells. Reticulin fibers appeared in a basket-like arrangement around both growing tips and epithelial sprouts, associated with a fainter staining for laminin. MMP-2 and MMP-9 activities were detected. MMP-2/MMP-9 expression decreased during the first week. Developing epithelial cords showed strong and difuse gelatinolytic activity. This activity coincided with the distribution of MMP-2 as determined by immunocytochemistry. On the other hand, MMP-9 was rather concentrated at the epithelial tips. These results suggest that gelatinolytic activity (with contribution of both MMP-2 and MMP-9) in the epithelium and at the epithelium-stroma interface are at least in part responsible for the tissue remodeling that allows epithelial growth and its projection into the surrounding stroma.

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Effects of castration and androgens upon prostatic proteoglycans in rats

Cited by 21 publications

References 7 publications

Apoptosis, tumour invasion and prostate cancer

Apoptosis, tumour invasion and prostate cancer

The role of growth factors in the suppression of active cell death in the prostate: an hypothesis

Localized matrix metalloproteinase (MMP)-2 and MMP-9 activity in the rat ventral prostate during the first week of postnatal development

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