Induction of Apoptosis by Castration in Epithelium of the Mouse Seminal Vesicles

Tanji, N.; Satoh, Hajime; Takagi-Morishita, Yayoi; Sugihara, Ayako; Terada, Nobuyuki; Cunha, Gerald R.; Yokoyama, M.

doi:10.1080/713828260

Cited by 2 publications

(4 citation statements)

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“…The number of proliferating cells based on Ki67 expression is 0.5% in SVs and 0.8% in the prostate (Laczko et al., 2005). Apoptotic cells are detected at frequency of 2.2% and 2% in the prostate and SV, respectively (Laczko et al., 2005; Tanji et al., 2003) and may increase with age (Jara et al., 2004). Based on these estimates, the tissue turnover time between the prostate and the SVs does not seem to differ considerably.…”

Section: Dna Damage In Prostate and Seminal Vesicle Epitheliummentioning

confidence: 99%

“…The prostate and SVs are androgen dependent in their organ development, secretory function and maintenance of epithelial structure (Tanji et al., 2003). Secretory and stromal cells of both tissues express AR (Laczko et al., 2005).…”

Section: Dna Damage In Prostate and Seminal Vesicle Epitheliummentioning

confidence: 99%

“…The studies have been limited by the fact that only a few models of the SV have been established, and the existing ones have mostly been applied to studies on the male reproductive function. Some in vivo studies have been carried out in mouse and rat models (Jara et al., 2004; Kumano et al., 2008; Tanji et al., 2003; Yeh et al., 2009). Primary epithelial SV cells have been isolated from rats and guinea pigs and used to study the secretory functions of the SVs (Kierszenbaum et al., 1983; Lieber et al., 1980).…”

Section: Introductionmentioning

confidence: 99%

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Maintenance of genomic integrity after DNA double strand breaks in the human prostate and seminal vesicle epithelium: The best and the worst

Jäämaa

Laiho

2012

Molecular Oncology

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Prostate cancer is one of the most frequent cancer types in men, and its incidence is steadily increasing. On the other hand, primary seminal vesicle carcinomas are extremely rare with less than 60 cases reported worldwide. Therefore the difference in cancer incidence has been estimated to be more than a 100,000-fold. This is astonishing, as both tissues share similar epithelial structure and hormonal cues. Clearly, the two epithelia differ substantially in the maintenance of genomic integrity, possibly due to inherent differences in their DNA damage burden and DNA damage signaling. The DNA damage response evoked by DNA double strand breaks may be relevant, as their faulty repair has been implicated in the formation of common genomic rearrangements such as TMPRSS2-ERG fusions during prostate carcinogenesis. Here, we review DNA damaging processes of both tissues with an emphasis on inflammation and androgen signaling. We discuss how benign prostate and seminal vesicle epithelia respond to acute DNA damage, focusing on the canonical DNA double strand break-induced ATM-pathway, p53 and DNA damage induced checkpoints. We propose that the prostate might be more prone to the accumulation of genetic aberrations during epithelial regeneration than seminal vesicles due to a weaker ability to enforce DNA damage checkpoints.

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Section: Dna Damage In Prostate and Seminal Vesicle Epitheliummentioning

confidence: 99%

Section: Dna Damage In Prostate and Seminal Vesicle Epitheliummentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Maintenance of genomic integrity after DNA double strand breaks in the human prostate and seminal vesicle epithelium: The best and the worst

Jäämaa

Laiho

2012

Molecular Oncology

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“…Mice were injected daily at 10 a.m. with vehicle only, TP (4 Vg/ g body weight) or with both TP (4 gg/g body weight) and ATRA (1-8 gg/g body weight) for 1-8 days. The group of mice in which only ATRA (1)(2)(3)(4)(5)(6)(7)(8) Vg/g body weight) was injected daily for 1-8 days was eliminated in the study, because preliminary data showed that ATRA at the various doses did not affect the development of SVs of castrated mice.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of all-trans retinoic acid on androgen-induced growth of mouse seminal vesicles in vivo and its mechanism

et al. 2005

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We examined the effect of all-trans retinoic acid (ATRA) on the androgen-induced growth of mouse seminal vesicles (SVs) in vivo and its mechanisms. Testosterone propionate (TP) alone or with ATRA was injected daily into adult castrated BALB/c mice. Injections of ATRA significantly inhibited the TP-induced growth of SVs in terms of wet weight and DNA synthesis by a pair of SVs evaluated by [3H]thymidine uptake. The bromodeoxyuridine labelling index showed that ATRA inhibited the proliferation of both epithelial and stromal cells. Immunoreactivity for retinoic acid receptor-a was found in the basal epithelial cells. Injections of ATRA affected neither 5a-reductase activity nor the expression of mRNAs for TGF-b1, 2 and 3 and TGF-b receptor 1 and 2 in the SVs. However, androgen receptor (AR) binding assays and Western blotting revealed a decrease in AR without a change in ligand-binding affinity. The present study showed that retinoid inhibited the androgen-induced growth of mouse SVs in vivo, and suggests that a decrease in AR is one of its mechanisms.

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Induction of Apoptosis by Castration in Epithelium of the Mouse Seminal Vesicles

Cited by 2 publications

References 0 publications

Maintenance of genomic integrity after DNA double strand breaks in the human prostate and seminal vesicle epithelium: The best and the worst

Maintenance of genomic integrity after DNA double strand breaks in the human prostate and seminal vesicle epithelium: The best and the worst

Inhibitory effect of all-trans retinoic acid on androgen-induced growth of mouse seminal vesicles in vivo and its mechanism

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