Paracrine-Mediated Apoptosis in Reproductive Tract Development

Roberts, Lori M.; Hirokawa, Yoshifumi; Nachtigal, Mark W.; Ingraham, Holly A.

doi:10.1006/dbio.1998.9190

Cited by 61 publications

(37 citation statements)

References 39 publications

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“…The expression of WT1 in the Mü llerian duct indicates that WT1 also might have a direct impact on Mü llerian duct regression. Interestingly, the AMH receptor was not found to be expressed in the epithelium of the Müllerian duct, but only in the surrounding interstitium and it was demonstrated that paracrine factors are involved in apoptosis of the Mü llerian ducts (Roberts et al 1999, Teixeira et al 2001. Since WT1 is known to play a role in apoptosis, it can be suggested that it might be implicated in the cellular crosstalk of Mü llerian duct regression (Menke et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Coexpression of Wilms’ tumor suppressor 1 (WT1) and androgen receptor (AR) in the genital tract of human male embryos and regulation of AR promoter activity by WT1

Köhler¹,

Delezoide²,

Boizet-Bonhoure³

et al. 2007

Journal of Molecular Endocrinology

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The Wilms' tumor suppressor 1 (WT1) is one of the key regulators of early male genital development. The androgen receptor (AR) is the major local factor responsible for the development of the male genitalia. As a subset of patients, with WT1 mutations and virilization defects, were found to present normal testosterone producing testes after birth, which suggests androgen resistance, we hypothesized that WT1 and AR might functionally interact during the development of the external genitalia. Coexpression of WT1 and AR was found in the mesenchyme surrounding the urogenital sinus, the mesonephros, and the Mü llerian duct at 7 weeks p.c. and in the epididimys, vas deferens, and the gubernaculum testes from 13 to 27 weeks p.c. in human male embryos. A modification of AR expression by WT1 (WT1C/C, WT1C/K, and WT1C/K R394W) was seen in CV1, Hela, LNCaP, and T293 cells. WT1 was shown to increase or decrease AR expression depending on the cell line (1.6-to 3.7-fold). In this study, we consider LNCaP and T293 cells as the most physiological cell system, as both originate from the human urogenital tract. In these cell lines, a repressional effect of the mutant WT1C/K R394W (0.5-fold) on AR expression in comparison to the wild-type WT1C/K could be demonstrated. From our data, we conclude that a functional interaction of WT1 and AR might play a role during the development of the male external genitalia, but as the regulatory effects were moderate most likely in concert with other local cofactors.

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Section: Discussionmentioning

confidence: 99%

Coexpression of Wilms’ tumor suppressor 1 (WT1) and androgen receptor (AR) in the genital tract of human male embryos and regulation of AR promoter activity by WT1

Köhler¹,

Delezoide²,

Boizet-Bonhoure³

et al. 2007

Journal of Molecular Endocrinology

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“…It is well described that AMH causes regression of the Müllerian duct by inducing cellular apoptosis (Roberts et al 1999). It is therefore interesting to speculate as to why the high concentrations in small follicles are not similarly damaging.…”

Section: Function Of Amh In the Normal Ovarymentioning

confidence: 96%

Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

Pellatt¹,

Rice²,

Mason³

2010

Reproduction

190

112

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Anti-Mü llerian hormone (AMH) was initially thought to be produced solely by the foetal male during sexual differentiation to promote regression of the Mü llerian ducts. Over the last decade, however, a new and interesting role has emerged for AMH in the ovary. In human ovaries, AMH is produced by granulosa cells from 36 weeks of gestation until menopause, with the highest expression being in small antral follicles. AMH production gradually declines as follicles grow; once follicles reach a size at which they are dominant, it has largely disappeared. Its removal from these larger follicles appears to be an important requirement for dominant follicle selection and progression to ovulation as AMH has an inhibitory role in the ovary, reducing both primordial follicle initiation and follicle sensitivity to FSH by inhibition of aromatase. It is for this reason that AMH is a focus of interest in polycystic ovary syndrome (PCOS). Serum levels are doubled, and granulosa cell production is greatly increased. Interestingly, there appear to be two groups of women with PCOS who can be distinguished by their AMH level: one group consists of those who have high levels which do not reduce with treatment and who respond less well to induction of ovulation, and a second group consists of those in whom the level is less elevated and reduces on treatment and who seem to respond rather better. Understanding the reason for the raised AMH in PCOS may give clues as to the mechanism of anovulation. To conclude, AMH appears to have a major inhibitory role during folliculogenesis, which may contribute to anovulation in PCOS.

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“…The MIS type I receptor has not been identified; however, bone morphogenic protein 1a is a strong candidate to be this receptor (5). Interaction between MIS and its receptor initiates a signal that ultimately causes regression of the mullerian ducts through apoptosis by a paracrine mechanism (6). Mutations in MIS or its type II receptor cause the human male sexual abnormalities, persistent mullerian duct syndrome and pseudohermaphroditism (7), and deletion of MIS or the MISRII also results in development of pseudohermaphroditism in mice (8,9).…”

mentioning

confidence: 99%

Synergistic Cooperation between the β-Catenin Signaling Pathway and Steroidogenic Factor 1 in the Activation of the Mullerian Inhibiting Substance Type II Receptor

Hossain

Saunders

2003

Journal of Biological Chemistry

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Mullerian inhibiting substance type II receptor (MISRII) is a member of the transforming growth factor-␤ superfamily. Mutations in mullerian inhibiting substance (MIS) or MISRII cause male sexual abnormalities, persistent mullerian duct syndrome, and pseudohermaphroditism. The spatial and temporal regulation of MIS and MISRII is important for its biological action. Male Wnt7a mutant mice do not undergo regression of mullerian ducts. Here we showed that the canonical Wnt signaling pathway regulated MISRII. The promoter MISRII was activated by ␤-catenin expression, and this activation was dependent on TCF4-binding sites. The nuclear receptor superfamily member steroidogenic factor 1 (SF1) synergistically activated the MISRII promoter with ␤-catenin. APC, a negative regulator of Wnt signaling, decreased SF1-mediated activation of the MISRII promoter in the colon carcinoma cell line SW480. We also showed a direct physical interaction between ␤-catenin and SF1 by co-immunoprecipitation. Thus, our findings suggest that MISRII is a developmental target of Wnt7a signaling for mullerian duct regression during sexual differentiation.

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Paracrine-Mediated Apoptosis in Reproductive Tract Development

Cited by 61 publications

References 39 publications

Coexpression of Wilms’ tumor suppressor 1 (WT1) and androgen receptor (AR) in the genital tract of human male embryos and regulation of AR promoter activity by WT1

Coexpression of Wilms’ tumor suppressor 1 (WT1) and androgen receptor (AR) in the genital tract of human male embryos and regulation of AR promoter activity by WT1

Anti-Müllerian hormone and polycystic ovary syndrome: a mountain too high?

Synergistic Cooperation between the β-Catenin Signaling Pathway and Steroidogenic Factor 1 in the Activation of the Mullerian Inhibiting Substance Type II Receptor

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