Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition.

Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Research Abstract Details 

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Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Abstract Text:

Eric Nilsson,Natalie Rogers,Michael K Skinner,

The oocytes found within the primordial follicles of mammalian ovaries remain quiescent for months to years until they receive the appropriate signals to undergo the primordial to primary follicle transition and initiate folliculogenesis. The molecular mechanisms and extracellular signaling factors that regulate this process remain to be fully elucidated. The current study investigates the mechanisms utilized by anti-Müllerian hormone (AMH; i.e. Müllerian inhibitory substance) to inhibit the primordial to primary follicle transition. Ovaries from 4-day-old rats were placed into organ culture and incubated in the absence or presence of AMH, either alone or in combination with known stimulators of follicle transition, including basic fibroblast growth factor (bFGF), kit ligand (KITL), or keratinocyte growth factor (KGF). Following 10 days of culture, the ovaries were sectioned, stained, and morphologically evaluated to determine the percentage of primordial versus developing follicles. As previously demonstrated, AMH treatment decreased primordial to primary follicle transition. Interestingly, AMH inhibited the stimulatory actions of KITL, bFGF, and KGF. Therefore, AMH can inhibit the basal and stimulated development of primordial follicles. To investigate the mechanism of AMH actions, the influence AMH has on the ovarian transcriptome was analyzed. AMH treatment when compared with controls was found to alter the expression of 707 genes. The overall effect of AMH exposure is to decrease the expression of stimulatory factors, increase the expression of inhibitory factors, and regulate cellular pathways (e.g. transforming growth factor beta signaling pathway) that result in the inhibition of primordial follicle development. Analysis of the regulatory factors and cellular pathways altered by AMH provides a better understanding of the molecular control of primordial follicle development.

Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Publishing Authors By Initials

E Nilsson,N Rogers,MK Skinner,

For similar peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta research

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Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Reproduction (Cambridge, England)

VOLUME: 134

Page Numbers: 209-21

Journal Abbreviation: Reproduction

ISSN: 1470-1626

DAY: 27

MONTH: Aug

YEAR: 2007

Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100966036

Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Keywords Mesh Terms:

KEYWORDS: Transforming Growth Factor beta

MESH TERMS: metabolism

Chemical & Substance for Abstract: Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition. Information

Substance Name: Anti-Mullerian Hormone

Registry Number: 80497-65-0

Grant and Affiliation Information for Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition.

AFFILIATION: Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-4231, USA.

Country: England

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MEDLINETA: Reproduction

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