Castration induced changes in dog prostate gland associated with diminished activin and activin receptor expression

Al-Omari, Ruba; Shidaifat, Falah; Dardaka, Mousa

doi:10.1016/j.lfs.2005.03.030

Cited by 14 publications

(11 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previously we have demonstrated that castration resulted in no changes in the proliferation pattern of basal cells and induced stromal cell proliferation [2]. However, the results of this study extended our previous investigation by showing that as the time progressed after castration there is a significant cessation of basal and stromal cell proliferation.…”

Section: Discussionsupporting

confidence: 72%

“…The immunohistochemistry was performed as previously described [2]. Five µM sections were picked on vecta bond (Vector labratoies, buringame, CA, USA) coated slides and were then deparaffinized in xylene and rehydrated in descending series of alcohol concentrations.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…Therefore, castration at any time during the male lifespan leads to a rapid involution of the gland which appeared to be due largely to a massive death of secretory epithelial cells. However, all other cellular components of the prostate gland also suffer different changes in response to androgen ablation which ranged from the cellular death to alteration in their proliferation and differentiation capacities [1,2]. These cellular components include basal cells, smooth muscles, and endothelial cells.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Effect of Castration on Extracellular Matrix Remodeling and Angiogenesis of the Prostate Gland

2007

Self Cite

View full text Add to dashboard Cite

Abstract. This study was conducted to evaluate the long term effect of castration on the prostate gland proliferation, extracellular matrix remodeling and angiogenesis. Prostate gland proliferation was assessed by immunolocalization of proliferating cell nuclear antigen (PCNA). The expression level of vascular endothelial growth factor (VEGF), transforming growth factor-β (TGF-β) and metaloprotenase-13 (MMP-13) by the prostate gland were assessed by immunohistochemistry and quantitative real-time PCR. The expression of the above mentioned parameters by the prostate gland of mature intact dogs were compared to that of castrated dogs six months post-castration. The results showed that castration induced a remarkable atrophy of the prostate gland which was associated with a highly significant decrease in the PCNA proliferation index. Although TGF-β protein was immunolocalized to the epithelial and stroma cells of the prostate gland from both intact and castrated dogs, castration induced a significant up-regulation of TGF-β mRNA expression. VEGF mRNA expression and its encoded protein immunolocalization were decreased significantly by the prostate gland from castrated dogs as compared to that of intact dogs. Castration, on the other hand, resulted in no significant change in MMP-13 mRNA expression despite an effect on its cellular immunolocalization which appeared to be localized to the epithelial and stromal cells of the prostate gland from castrated dogs as compared to epithelial cells of the prostate gland from intact dogs. These results indicated that castration-induced prostate gland regression continued to exert a potent suppressive effect on prostate gland proliferation which might be mediated by the elevated level of TGF-β. Moreover, the low expression level of VEGF might reflect a reduced blood flow demand by the regressed and growthdormant prostate after castration.

show abstract

Section: Discussionsupporting

confidence: 72%

Section: Immunohistochemistrymentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Effect of Castration on Extracellular Matrix Remodeling and Angiogenesis of the Prostate Gland

2007

Self Cite

View full text Add to dashboard Cite

show abstract

“…Evidence supporting this proposal was the different expression and localization of inhibin a and b subunits by normal, malignant, and benign prostatic cells. Whereas inhibin bA subunit and dimeric activin have been shown to be expressed by normal [9,10], malignant [11], benign [12] and prostate cancer cell lines [13], inhibin a has been shown to be expressed by normal differentiated epithelial cells only [9,14] in benign prostate hyperplasia and in non-malignant regions of prostate carcinoma [15]. Expression of inhibin a by malignant prostatic cells or prostate cancer cell lines has not been detected [15].…”

Section: Introductionmentioning

confidence: 99%

“…On the other hand, activin regulation of prostate gland growth seemed to involve interaction with androgens. In this context it has been shown that activin expression by the epithelial cells of the prostate gland is suppressed by androgen withdrawal [10] and that activin inhibits androgen-stimulated prostate gland morphogenesis [14] and suppresses androgen-induced LNCap cell proliferation [21].…”

Section: Introductionmentioning

confidence: 99%

Interaction of testosterone with inhibin α and βA subunits to regulate prostate gland growth

Shidaifat

Al-Zuhair

Ismail

2007

Endocr

Self Cite

View full text Add to dashboard Cite

Testosterone regulation of prostate gland growth has been shown to involve reciprocal interaction with inhibin and activin. This study was therefore conducted to correlate the effect of testosterone on prostate gland proliferation and differentiation with the level of expression of inhibin alpha and betaA subunits. Immature dogs were treated with testosterone for 0, 3, 7, and 14 days and prostate gland growth was assessed by morphological and immunohistological localization of differentiation and proliferation markers. The results showed that testosterone treatment resulted in an initial significant increase in PCNA proliferation index by days 3 and 7, followed by a significant decrease by day 14 post-treatment. Interestingly, the decrease of cell proliferation was associated with structural and biochemical changes characteristic of glandular and stromal differentiation of the prostate gland. These changes include progressive glandular ductal canalization and inter-ductal stroma differentiation which were apparent from a gradual shift from vimentin expression to vimentin and alpha-actin expression. Testosterone also had a differential effect on inhibin alpha and beta subunits. Although testosterone treatment resulted in significant and constant inhibition of alpha subunit mRNA expression, it resulted in a significant increase of betaA mRNA expression by day 3, followed by a decrease by days 7 and 14. These results indicated that testosterone acts first to drive proliferation of undifferentiated prostatic cells and then to maintain a low proliferation turnover of differentiated cells. Because it has been shown that activin is an antagonistic regulator of androgens, the attenuated stimulatory effect of testosterone on cell proliferation by day 14 might be mediated, at least in part, by interplay between testosterone and activin.

show abstract

Activins, Inhibins, and Bone Morphogenetic Proteins as Modulators and Biomarkers of Prostate Cancer Progression

Hayashida

Gupta

Thiagalingam

et al. 2008

Transforming Growth Factor-Β in Cancer Therapy, Volume I

View full text Add to dashboard Cite

Castration induced changes in dog prostate gland associated with diminished activin and activin receptor expression

Cited by 14 publications

References 26 publications

Effect of Castration on Extracellular Matrix Remodeling and Angiogenesis of the Prostate Gland

Effect of Castration on Extracellular Matrix Remodeling and Angiogenesis of the Prostate Gland

Interaction of testosterone with inhibin α and βA subunits to regulate prostate gland growth

Activins, Inhibins, and Bone Morphogenetic Proteins as Modulators and Biomarkers of Prostate Cancer Progression

Contact Info

Product

Resources

About