scholarly journals Anti-Müllerian hormone: a new marker for ovarian function

Reproduction ◽  
2006 ◽  
Vol 131 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Jenny A Visser ◽  
Frank H de Jong ◽  
Joop S E Laven ◽  
Axel P N Themmen
Keyword(s):  
Transforming Growth Factor ◽  
Ovarian Function ◽  
Ovarian Follicle ◽  
Primordial Follicle ◽  
Transforming Growth Factor Β ◽  
Inhibitory Effect ◽  
Quantitative Aspect ◽  
Specific Expression ◽  
Differentiation Factors ◽  
Specific Expression Pattern

Anti-Müllerian hormone (AMH) is a member of the transforming growth factor β family of growth and differentiation factors. In the ovary, AMH has an inhibitory effect on primordial follicle recruitment as well as on the responsiveness of growing follicles to follicle-stimulating hormone (FSH). The ovary-specific expression pattern in granulosa cells of growing nonselected follicles makes AMH an ideal marker for the size of the ovarian follicle pool. This review summarizes recent findings concerning AMH and its role as a marker for the quantitative aspect of ovarian reserve as well as ovarian dysfunction.

scholarly journals Role of Anti-Müllerian Hormone in Gynecology: A Review of Literature

2015 ◽  
Vol 6 (2) ◽  
pp. 51-61 ◽  
Author(s):  
Naina Kumar ◽  
Amit Kant Singh
Keyword(s):  
English Language ◽  
Transforming Growth Factor ◽  
Recent Literature ◽  
Ovarian Follicle ◽  
Primordial Follicle ◽  
Review Of Literature ◽  
Specific Expression ◽  
Specific Expression Pattern ◽  
Protein Part

ABSTRACT Anti-müllerian hormone (AMH) or Müllerian inhibiting substance (MIS), is a dimeric protein part of the transforming growth factor (TGF)-beta subfamily. It plays two important roles in follicle genesis. First, it delays entrance of primordial follicle into pool of follicles in growth and secondly, it decreases the sensitivity of ovarian follicle toward follicle-stimulating hormone (FSH). The ovary-specific expression pattern in granulosa cells of growing non-selected follicles makes AMH an ideal marker for size of the ovarian follicle pool. This review summarizes recent literature concerning AMH and its role in various gynecological conditions. Methods The literature regarding AMH was searched from various English language journals and published peer-reviewed articles on Pubmed, MEDLINE and Google Scholar till 2014. How to cite this article Kumar N, Singh AK. Role of Antimüllerian Hormone in Gynecology: A Review of Literature. Int J Infertil Fetal Med 2015;6(2):51-61.

scholarly journals Inhibitor of Differentiation (Id) Genes Are Expressed in the Steroidogenic Cells of the Ovine Ovary and Are Differentially Regulated by Members of the Transforming Growth Factor-β Family

Endocrinology ◽  
2009 ◽  
Vol 151 (3) ◽  
pp. 1247-1256 ◽  
Author(s):  
Kirsten Hogg ◽  
Sophie L. Etherington ◽  
Julia M. Young ◽  
Alan S. McNeilly ◽  
W. Colin Duncan
Keyword(s):  
Gene Expression ◽  
Transforming Growth Factor ◽  
Ovarian Follicle ◽  
Transforming Growth Factor Β ◽  
Differential Staining ◽  
Tgfβ Signaling ◽  
Specific Expression ◽  
Id Proteins ◽  
Thecal Cells

Inhibitor of differentiation (Id) proteins act during embryogenesis and development to repress gene transcription required for lineage commitment, while promoting cell growth. Growth factors belonging to the TGFβ superfamily of signaling molecules, notably the bone morphogenetic proteins (BMPs) and activin, can regulate Id expression in these tissues. Id expression and function in adult physiology is less well determined, and we hypothesized a role for Id proteins in the adult mammalian ovary. Immunohistochemistry for Id1, Id2, Id3, and Id4 in the sheep ovary revealed consistent expression in granulosa and thecal cells of ovarian follicles throughout development. In atretic follicles, Id proteins were selectively down-regulated in thecal cells (P < 0.0001). Additionally, Id1 was universally up-regulated in the cumulus cells adjacent to the oocyte. Immunohistochemistry for phospho (p)-smad 1/5/8 signaling components (stimulated by BMPs) showed a punctate pattern of expression whereas p-smad 2/3 (stimulated by activin) was ubiquitously expressed in follicles. Neither pathway, however, displayed differential staining in line with Id1 cumulus-specific expression, suggesting a more complex relationship between Id1 expression and TGFβ signaling in these cells. Nevertheless, in vitro, stimulation of ovine granulosa cells with BMP6 or activin A led to a respective increase and decrease in Id1 (P < 0.0001), Id2 (P < 0.0001), Id3 (P < 0.0001), and Id4 (P < 0.05) transcripts, and Id1 gene expression was further manipulated by the oocyte-secreted factors BMP15 and growth differentiation factor 9 (P < 0.001). These data confirm that TGFβ signaling can regulate Id gene expression in the sheep ovarian follicle and suggest a functional role for the Id family in the mammalian ovary.

scholarly journals Mechanism of Transforming Growth Factor β–induced Inhibition of T Helper Type 1 Differentiation

2002 ◽  
Vol 195 (11) ◽  
pp. 1499-1505 ◽  
Author(s):  
Leonid Gorelik ◽  
Stephanie Constant ◽  
Richard A. Flavell
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Inhibitory Effect ◽  
Interleukin 12 ◽  
T Helper ◽  
Retroviral Transduction ◽  
Cell Functions ◽  
Proliferation And Differentiation ◽  
Direct Inhibitory Effect

Regulation by transforming growth factor (TGF)-β plays an important role in immune homeostasis. TGF-β inhibits T cell functions by blocking both proliferation and differentiation. Here we show that TGF-β blocks Th1 differentiation by inhibiting the expression of T-bet, the apparent masterregulator of T helper (Th)1 differentiation. Restoration of T-bet expression through retroviral transduction of T-bet into developing Th1 cells abrogated the inhibitory effect of TGF-β. In addition, we show that, contrary to prior suggestions, downregulation of interleukin 12 receptor β2 chain is not key to the TGF-β–mediated effect. Furthermore, we show that the direct inhibitory effect of TGF-β on T cells is responsible, at least in part, for the inability of BALB/c mice to mount a Leishmania-specific Th1 response and to clear Leishmanial infection.

Serum-stimulated α1 type IV collagen gene transcription is mediated by TGF-β and inhibited by estradiol

1998 ◽  
Vol 274 (2) ◽  
pp. F252-F258 ◽  
Author(s):  
Jun Lei ◽  
Sharon Silbiger ◽  
Fuad N. Ziyadeh ◽  
Joel Neugarten
Keyword(s):  
Growth Factor ◽  
Gene Transcription ◽  
Type Iv Collagen ◽  
Transforming Growth Factor ◽  
Combined Treatment ◽  
Calf Serum ◽  
Neutralizing Antibody ◽  
Transforming Growth Factor Β ◽  
Inhibitory Effect ◽  
Type Iv

We examined the hypothesis that fetal calf serum (FCS) stimulates murine mesangial cell α1 type IV collagen ( COL4A1) gene transcription by increasing autocrine production of transforming growth factor-β (TGF-β) through a platelet-derived growth factor (PDGF)-dependent mechanism. PDGF-stimulated COL4A1 gene transcription was inhibited by neutralizing antibody to TGF-β (119.3 ± 3.6 vs. 106.0 ± 6.2 relative luciferase units, expressed as a percentage of control untreated cells, P < 0.003). FCS-stimulated gene transcription was inhibited by neutralizing antibody to PDGF (148.3 ± 4.1 vs. 136.7 ± 0.3 relative luciferase units, P < 0.002) and by neutralizing antibody to TGF-β (148.3 ± 4.1 vs. 127.1 ± 3.4 relative luciferase units, P < 0.036). The inhibitory effect of combined treatment with anti-PDGF and anti-TGF-β antibody on gene transcription was no greater than that of anti-TGF-β antibody alone [129.5 ± 0.53 vs. 127.1 ± 3.4 relative luciferase units, P = not significant (NS)]. FCS-stimulated gene transcription was also inhibited by estradiol (10−7 M) (148.4 ± 3.1 vs. 119.4 ± 8.1 relative luciferase units, P < 0.019). In the presence of estradiol, anti-TGF-β antibody failed to further reduce serum-stimulated gene transcription (119.4 ± 8.1 vs. 115.6 ± 9.8, P = NS), suggesting that estradiol reverses FCS-stimulated COL4A1 gene transcription by antagonizing the actions of TGF-β. Measurement of type IV collagen synthesis by Western blotting confirmed that the intact gene responded in a manner analogous to the promoter construct.

scholarly journals SMAD3 regulates the diverse functions of rat granulosa cells relating to the FSHR/PKA signaling pathway

Reproduction ◽  
2013 ◽  
Vol 146 (2) ◽  
pp. 169-179 ◽  
Author(s):  
Yexia Li ◽  
Yujie Jin ◽  
Yuxia Liu ◽  
Chunyan Shen ◽  
Jingxia Dong ◽  
...  
Keyword(s):  
Granulosa Cells ◽  
Transforming Growth Factor ◽  
Ovarian Follicle ◽  
Transforming Growth Factor Β ◽  
Female Rats ◽  
Nuclear Antigen ◽  
Follicle Development ◽  
Sprague Dawley ◽  
Ovarian Follicle Development ◽  
Estrogen Production

The function of Smad3, a downstream signaling protein of the transforming growth factor β (TGFβ) pathway, in ovarian follicle development remains to be elucidated. The effects of Smad3 on ovarian granulosa cells (GCs) in rat were studied. Female rats (21 days of age Sprague–Dawley) received i.p. injections of pregnant mare serum gonadotropin, and GCs were harvested for primary culture 48 h later. These cells were engineered to overexpress or knockdown Smad3, which were validated by immunohistochemistry and western blot. The expression of proliferating cell nuclear antigen (PCNA), cyclin D2, TGFβ receptor II (TGFβRII), protein kinase A (PKA), and FSH receptor (FSHR) was also detected by western blotting. Cell cycle and apoptosis of GCs were assayed by flow cytometry. The level of estrogen secreted by GCs was detected by ELISA. Smad3 overexpression promoted estrogen production and proliferation while inhibiting apoptosis of GCs. Reduction in Smad3 by RNAi resulted in reduced estrogen production and proliferation and increased apoptosis of GCs. Manipulation of Smad3 expression also resulted in changes in FSHR and PKA expression, suggesting that the effects of Smad3 on follicle development are related to FSHR-mediated cAMP signaling.

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