Inhibin and Activin Locally Regulate Rat Ovarian Folliculogenesis

Woodruff, Teresa K.; Lyon, Rebecca; Hansen, Stanley E.; Rice, Glenn C.; Mather, Jennie P.

doi:10.1210/endo-127-6-3196

Cited by 248 publications

(142 citation statements)

References 44 publications

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“…Intrabursal injection of Activin A has been reported to increase the number of atretic follicles and decrease granulosa cell proliferation [35]. The results presented here indicate that the increased proportion of non-growing follicles observed in 50 ng/ml Activin (54%) compared to control group (26%) was not due to an increase in atresia since no differences in total numbers or viability were detected between groups suggesting that the reduction of the growing follicle in Activin A (50 ng/ml) group is a result of growth inhibition.…”

Section: Discussionmentioning

confidence: 99%

Activin A inhibits activation of human primordial follicles in vitro

Ding

Thong

Krishna

et al. 2010

J Assist Reprod Genet

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Purpose To determine whether Activin A affects the activation and survival of human primordial follicles in vitro. Methods Ovarian cortical biopsies from eight women undergoing elective caesarean sections or benign gynaecological procedures were taken and cut into small pieces (1-3 mm 3 ), cultured in serum-free medium for 7 days with/without human recombinant Activin A at a concentration of either 50 or 100 ng/ml. Ovarian tissue were analysed by histology for follicle viability, development and density. Result(s) Significant activation of primordial follicles within cultured cortical tissue was observed after 7 days in control medium. However, medium supplemented with Activin A at 50 ng/ml resulted in significant inhibition of follicular activation. Increasing the concentration of Activin A to 100 ng/ml reversed the inhibitory effect. The effect of Activin A appeared to be specific to activation of non-growing (primordial) follicles into the growing population since no significant differences in follicle viability was observed between treatment groups. Conclusion(s) Activin A at a concentration of 50 ng/ml can inhibit the spontaneous activation of human primordial follicles in vitro indicating that this may be a component of the signalling mechanisms that maintain follicular quiescence.

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Section: Discussionmentioning

confidence: 99%

Activin A inhibits activation of human primordial follicles in vitro

Ding

Thong

Krishna

et al. 2010

J Assist Reprod Genet

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show abstract

“…LH surge is associated with decrease in the expression of the inhibin subunits and after formation of CL, expression of α and β A subunits are maintained in primates. Inhibin exerts stimulatory effects on folliculogenesis and may control follicular growth, development, atresia, oocyte maturation and spermatogenesis [73,74]. Mice bearing a targeted deletion of the α-subunit gene generated by homologous recombination in mouse embryonic stem cells develop normally, but all of them eventually develop mixed or incompletely differentiated gonadal stromal tumors [1].…”

Section: Inhibins and Its Role In Tumourigenesismentioning

confidence: 99%

New targets for old hormones: inhibins clinical role revisited [Review]

2011

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Abstract. Inhibins are gonadal peptide hormones belonging to the transforming growth factor-β (TGF-β) superfamily that regulate the pituitary follicle stimulating hormone (FSH) secretion by negative feedback mechanisms. It is evident that the understanding of inhibins function in the hypothalamic-pituitary-gonadal axis will provide insights into physiology and pathology of the gonadal function. In recent years, a great deal of attention has been focussed on clinical relevance of measuring circulating inhibins in normal and disease state. The past few years also have witnessed the emergence and discovery of extra pituitary action of inhibins that might provide further insights into the underlying diseases like cancer especially in the reproductive axis and various other new endocrine target organs. In this review after systematic analysis of literature, we discuss briefly the known and recent advances in function of these hormones highlighting also its structure, production and mechanisms of signal transduction. Also this review discusses about the physiological relevance of inhibin association in the normal function to the development of reproductive cancers. Finally, we describe evidence from various emerging studies that inhibins make an important contribution to other physiological functions apart from reproduction which reveals new endocrine target organs of inhibins. The emerging view is inhibin participates in multiple ways to regulate the function in different cell types and still complete repertoire of its actions is under investigation. Key words: Inhibin, Transforming growth factor, Ovarian cancer, Activins, BetaglycanMAMMAliAn reproduction is intricate, highly ordered and is coordinated by assorted neural, neuroendocrine, endocrine, autocrine and paracrine cell-cell communication pathways. Many of the pioneering discoveries meticulously demonstrated the roles of hypothalamic gonadotropin releasing hormone (GnRH) that stimulates pituitary gonadotropins such as follicle stimulating hormone (FSH) and leutinizing hormone (LH), which directly control gonadal functions. Subsequent breakthroughs in the advancement of molecular biology and in understanding signal transduction mechanisms suggested involvement of various cytokines and growth factors at each level of the hypothalamic-pituitary-gonadal axis in the paracrine/autocrine control of different programmed reproductive events. Members include inhibins and activins, belonging to the transforming growth factor (TGF-β) super family and follistatin (FS), a structurally distinct though functionally related molecule. It has been more than 70 years since the identification of negative feedback control of pituitary FSH secretion by inhibins. These factors also were shown to act in autocrine, endocrine or paracrine manner within the reproductive tissues, but the identification of specific pathways in different cellular context along the gonadal axis is still quite unclear and should thus be further investigated. The discovery process of extra pituitary action of ...

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“…Delineation of an intracellular signalling pathway for inhibin awaits unequivocal proof of a receptor for inhibin, about which controversy regarding its very existence persists. The evidence presented supporting the existence of an inhibin receptor is based on the identification of specific binding sites for inhibin on ovarian granulosa cells and Leydig cells (Woodruff et al 1990, Krummen et al 1994. Additional supporting data for the existence of a specific receptor include the demonstration of an inhibin-specific protein complex, k562, in haematopoietic cell lines (Lebrun & Vale 1997) and tumour-derived inhibin receptor proteins in the Matzuk inhibin knockout mice (Draper et al 1998).…”

Section: Inhibin and Activin Receptors And Signallingmentioning

confidence: 99%

The role of inhibins and activins in prostate cancer pathogenesis.

Dowling¹,

Risbridger²

2000

Endocrine-Related Cancer

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Successful prostate cancer diagnosis and management continue to provide challenges for the clinician. While interventions aimed at the containment of both early and late disease continue to fail in a significant number of patients, the search for answers must incorporate an analysis of the processes of normal and aberrant growth and development within the gland itself. Inhibin and its structurally related protein, activin, are members of the transforming-growth-factor β (TGFβ) superfamily. Originally identified as regulators of FSH, these proteins are now recognised to have widespread biological functions. This might be expected of proteins that are structurally homologous to TGFβ itself, which is recognised to have regulatory roles in both normal and malignant prostate tissue. The aim of this review is to examine the relationship between inhibins, activins and their related proteins and the development of prostate cancer. The homology with TGF, the pluripotent effects of activin on various tissues and the roles for inhibins in ovarian cancer make activins and inhibins candidate growth factors for involvement at multiple sites in the progression from benign disease to cancer. In compiling this review, we aim to delineate the changes in inhibins and activins in this pathway and in doing so implicate their potential roles in the progression of carcinogenesis. We will compare the changes in inhibin and its related proteins in prostate cancer to those that are known in ovarian cancer. We will discuss the similarities and differences between the putative role of activins and TGFβ in prostate carcinogenesis. The importance of this review lies in demonstrating that inhibin, an endocrine hormone, and its related proteins may contribute to endocrine-related cancers, such as that of the prostate gland.

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Inhibin and Activin Locally Regulate Rat Ovarian Folliculogenesis

Cited by 248 publications

References 44 publications

Activin A inhibits activation of human primordial follicles in vitro

Activin A inhibits activation of human primordial follicles in vitro

New targets for old hormones: inhibins clinical role revisited [Review]

The role of inhibins and activins in prostate cancer pathogenesis.

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