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Nathalie Di Clemente - One of the best experts on this subject based on the ideXlab platform.

  • Anti-Müllerian Hormone production in the ovary: a comparative study in bovine and porcine granulosa cells†.
    Biology of reproduction, 2020
    Co-Authors: Anthony Estienne, Nathalie Di Clemente, Danielle Monniaux, Peggy Jarrier, Christophe Staub, Eric Venturi, Yves Le Vern, Philippe Monget
    Abstract:

    In this study, we aimed to determine the origin of the difference, in terms of Anti-Mullerian Hormone production, existing between the bovine and porcine ovaries. We first confirmed by quantitative real-time-Polymerase-Chain Reaction, ELISA assay and immunohistochemistry that Anti-Mullerian Hormone mRNA and protein production are very low in porcine ovarian growing follicles compared to bovine ones. We then have transfected porcine and bovine granulosa cells with vectors containing the luciferase gene driven by the porcine or the bovine Anti-Mullerian Hormone promoter. These transfection experiments showed that the porcine Anti-Mullerian Hormone promoter is less active and less responsive to bone morphogenetic protein stimulations than the bovine promoter in both porcine and bovine cells. Moreover, bovine but not porcine granulosa cells were responsive to bone morphogenetic protein stimulation after transfection of a plasmidic construction including a strong response element to the bone morphogenetic proteins (12 repetitions of the GCCG sequence) upstream of the luciferase reporter gene. We also showed that SMAD6, an inhibitor of the SMAD1-5-8 pathway, is strongly expressed in porcine compared to the bovine granulosa cells. Overall, these results suggest that the low expression of Anti-Mullerian Hormone in porcine growing follicles is due to both a lack of activity/sensitivity of the porcine Anti-Mullerian Hormone promoter, and to the lack of responsiveness of porcine granulosa cells to bone morphogenetic protein signaling, potentially due to an overexpression of SMAD6 compared to bovine granulosa cells. We propose that the low levels of Anti-Mullerian Hormone in the pig would explain the poly-ovulatory phenotype in this species.

  • Dysregulation of the Anti-Mullerian Hormone system by steroids in women with polycystic ovary syndrome
    Journal of Clinical Endocrinology and Metabolism, 2017
    Co-Authors: Alice Pierre, Joëlle Taieb, Frank Giton, Michael Grynberg, Salma Touleimat, Hady El Hachem, Renato Fanchin, Danielle Monniaux, Joëlle Cohen-tannoudji, Nathalie Di Clemente
    Abstract:

    Context: Anti-Mullerian Hormone (AMH) and AMH type II receptor (AMHR2) are overexpressed in granulosa cells (GCs) from women with polycystic ovary syndrome (PCOS), the most common cause of female infertility. Objective: The aim of the study was to compare the regulation of the AMH/AMHR2 system by 5adihydrotestosterone (5a-DHT) and estradiol (E2) in GCs from control subjects and women with PCOS. Design, Setting, Patients: Experiments were performed on follicular fluids (FF) and GCs from women undergoing in vitro fertilization. Main Outcome Measures: FF steroid levels were measured by mass spectrometry, and messenger RNA (mRNA) accumulation was quantified by reverse transcription real-time polymerase chain reaction. Results: Total testosterone (T), free T, and 5 alpha-DHT FF levels were significantly higher (P < 0.001) in women with PCOS than in controls. However, E2 and sex Hormone-binding globulin concentrations were comparable between the two groups. In GCs from control women, the AMH and AMHR2 expression were not affected by 5a-DHT treatment, whereas AMH mRNA levels were upregulated by 5a-DHT in GCs from patients with PCOS (2.3-fold, P < 0.01) overexpressing the androgen receptor (1.4-fold, P < 0.05). E2 downregulated the AMH and AMHR2 expression in GCs from control women (1.4-fold, P < 0.001 and 1.8-fold, P < 0.01, respectively) but had no effect on these genes in GCs from women with PCOS. This differential effect of E2 was associated with a higher estrogen receptor 1 expression in GCs from women with PCOS (1.9-fold, P < 0.05). Conclusions: In GCs from women with PCOS, the regulation of AMH and AMHR2 expression is altered in a way that promotes the overexpression of the AMH/AMHR2 system, and could contribute to the follicular arrest observed in these patients.

  • Deregulation of Anti-Mullerian Hormone/BMP and transforming growth factor-{beta} pathways in Leydig cell lesions developed in male heterozygous multiple endocrine Neoplasia type 1 mutant mice
    Endocrine-Related Cancer, 2008
    Co-Authors: Nader Hussein, Nathalie Di Clemente, Huguette Casse, Sandra Fontanière, Anne-marie Morera, Séverine Mazaud Guittot, Alain Calender, Chang Zhang
    Abstract:

    Multiple endocrine neoplasia type 1 (MEN1) results from the mutation of the predisposing gene, MEN1. Heterozygous Men1 mutant mice previously generated by several laboratories, including ours, mimic largely MEN1 pathology. Interestingly, our heterozygous Men1 mutant mice exhibit not only the endocrine tumours commonly seen in MEN1 patients, but also Leydig cell tumours (LCT) with high frequency, accompanied systematically by loss of the wild-type Men1 allele. As there exists a similarity of tumour phenotype between these mice and those mutated for the components of Anti-Mullerian Hormone (AMH)/bone morphogenic protein (BMP) pathway belonging to transforming growth factor-beta (TGF-beta) family, we investigated the expression and the activity of this pathway, known to have an important biological role in Leydig cells. Here, we report that the expression of AMH receptor type 2 is reduced in Men1 LCTs. Both immunostaining and western blot analyses also demonstrate a markedly decreased nuclear expression of Smad1, 3, 4 and 5 in the tumours. More interestingly, we show that the reconstituted menin expression in Men1-deficient Leydig cells derived from LCTs can significantly increase the transcriptional activity of a BMP pathway target promoter, XVent2. Furthermore, we found that the expression of p18, p27 and cyclin dependant kinase 4 (Cdk4), targets of TGF-beta pathways, is altered in the Leydig cell lesions. Our data provide the evidence of the deregulation of AMH/BMP and TGF-beta pathways in mouse Men1 LCTs, highlighting their involvement in tumorigenesis of Leydig cells due to Men1 inactivation.

  • Anti-Müllerian Hormone
    Encyclopedia of Endocrine Diseases, 2004
    Co-Authors: Nathalie Josso, Nathalie Di Clemente
    Abstract:

    Anti-Mullerian Hormone, also called Mullerian inhibiting substance, is a member of the transforming growth factor-β family, whose main effect is the initiation of regression of the Mullerian ducts in the male fetus.

  • Ovarian Granulosa Cell Tumors Express a Functional Membrane Receptor for Anti-Müllerian Hormone in Transgenic Mice
    Endocrinology, 2001
    Co-Authors: Martin Dutertre, Jean-yves Picard, Lucile Gouédard, Françoise Xavier, Wen-qing Long, Nathalie Di Clemente, Rodolfo A. Rey
    Abstract:

    Anti-Mullerian Hormone inhibits granulosa cell growth and function. Both Anti-Mullerian Hormone and its type II receptor are expressed in normal granulosa cells. We show by histologic and molecular analyses that ovarian tumors developing in transgenic mice, obtained by targeted oncogenesis using an Anti-Mullerian Hormone promoter-SV40 oncogene construct, are of granulosa-cell origin. Because tissue-specific, cell-surface molecules are of particular interest for the analysis and treatment of tumors, we examined the expression of Anti-Mullerian Hormone type II receptor in the ovaries of these transgenic mice. We demonstrate that the Anti-Mullerian Hormone type II receptor is expressed not only in normal ovarian follicles, but also in granulosa cell tumors. Using a cell line derived from one of these tumors, we show that the Anti-Mullerian Hormone type II receptor protein is present on the surface of tumor cells and binds Anti-Mullerian Hormone. Furthermore, we show that the Anti-Mullerian Hormone receptor i...

Pierrick Haffray - One of the best experts on this subject based on the ideXlab platform.

  • Characterization of a Y‐specific duplication/insertion of the anti‐Mullerian Hormone type II receptor gene based on a chromosome‐scale genome assembly of yellow perch, Perca flavescens
    Molecular Ecology Resources, 2020
    Co-Authors: Romain Feron, Margot Zahm, Cédric Cabau, Christophe Klopp, Céline Roques, Olivier Bouchez, Camille Eché, Sophie Valière, Cécile Donnadieu, Pierrick Haffray
    Abstract:

    Yellow perch, Perca flavescens, is an ecologically and economically important species native to a large portion of the northern United States and southern Canada and is also a promising candidate species for aquaculture. However, no yellow perch reference genome has been available to facilitate improvements in both fisheries and aquaculture management practices. By combining Oxford Nanopore Technologies long-reads, 10X Genomics Illumina short linked reads and a chromosome contact map produced with Hi-C, we generated a high-continuity chromosome-scale yellow perch genome assembly of 877.4 Mb. It contains, in agreement with the known diploid chromosome yellow perch count, 24 chromosome-size scaffolds covering 98.8% of the complete assembly (N50 = 37.4 Mb, L50 = 11). We also provide a first characterization of the yellow perch sex determination locus that contains a male-specific duplicate of the Anti-Mullerian Hormone type II receptor gene (amhr2by) inserted at the proximal end of the Y chromosome (chromosome 9). Using this sex-specific information, we developed a simple PCR genotyping assay which accurately differentiates XY genetic males (amhr2by ) from XX genetic females (amhr2by ). Our high-quality genome assembly is an important genomic resource for future studies on yellow perch ecology, toxicology, fisheries and aquaculture research. In addition, characterization of the amhr2by gene as a candidate sex-determining gene in yellow perch provides a new example of the recurrent implication of the transforming growth factor beta pathway in fish sex determination, and highlights gene duplication as an important genomic mechanism for the emergence of new master sex determination genes.

  • Characterization of a Y-specific duplication/insertion of the Anti-Mullerian Hormone type II receptor gene based on a chromosome-scale genome assembly of yellow perch, Perca flavescens
    2019
    Co-Authors: Romain Feron, Margot Zahm, Cédric Cabau, Christophe Klopp, Céline Roques, Olivier Bouchez, Camille Eché, Sophie Valière, Cécile Donnadieu, Pierrick Haffray
    Abstract:

    Background: Yellow perch, Perca flavescens, is an ecologically and commercially important species native to a large portion of the northern United States and southern Canada. It is also a promising candidate species for aquaculture. No yellow perch reference genome, however, has been available to facilitate improvements in both fisheries and aquaculture management practices. Findings: By combining Oxford Nanopore Technologies long-reads, 10X genomics Illumina short linked reads and a chromosome contact map produced with Hi-C, we generated a high-continuity chromosome scale yellow perch genome assembly of 877.4 Mb. It contains, in agreement with the known diploid chromosome yellow perch count, 24 chromosome-size scaffolds covering 98.8% of the complete assembly (N50 = 37.4 Mb, L50 = 11). Genome annotation identified 41.7% (366 Mb) of repeated elements and 24,486 genes including 16,579 genes (76.3%) significantly matching with proteins in public databases. We also provide a first characterization of the yellow perch sex determination locus that contains a male-specific duplicate of the Anti-Mullerian Hormone type II receptor gene (amhr2by) inserted at the proximal end of the Y chromosome (chromosome 9). Using this sex-specific information, we developed a simple PCR genotyping test which accurately differentiates XY genetic males (amhr2by+) from XX genetic females (amhr2by−). Conclusions: Our high-quality genome assembly is an important genomic resource for future studies on yellow perch ecology, toxicology, fisheries, and aquaculture research. In addition, the characterization of the amhr2by gene as a candidate sex determining gene in yellow perch provides a new example of the recurrent implication of the transforming growth factor beta pathway in fish sex determination, and highlights gene duplication as an important genomic mechanism for the emergence of new master sex determination genes.

Romain Feron - One of the best experts on this subject based on the ideXlab platform.

  • Characterization of a Y‐specific duplication/insertion of the anti‐Mullerian Hormone type II receptor gene based on a chromosome‐scale genome assembly of yellow perch, Perca flavescens
    Molecular Ecology Resources, 2020
    Co-Authors: Romain Feron, Margot Zahm, Cédric Cabau, Christophe Klopp, Céline Roques, Olivier Bouchez, Camille Eché, Sophie Valière, Cécile Donnadieu, Pierrick Haffray
    Abstract:

    Yellow perch, Perca flavescens, is an ecologically and economically important species native to a large portion of the northern United States and southern Canada and is also a promising candidate species for aquaculture. However, no yellow perch reference genome has been available to facilitate improvements in both fisheries and aquaculture management practices. By combining Oxford Nanopore Technologies long-reads, 10X Genomics Illumina short linked reads and a chromosome contact map produced with Hi-C, we generated a high-continuity chromosome-scale yellow perch genome assembly of 877.4 Mb. It contains, in agreement with the known diploid chromosome yellow perch count, 24 chromosome-size scaffolds covering 98.8% of the complete assembly (N50 = 37.4 Mb, L50 = 11). We also provide a first characterization of the yellow perch sex determination locus that contains a male-specific duplicate of the Anti-Mullerian Hormone type II receptor gene (amhr2by) inserted at the proximal end of the Y chromosome (chromosome 9). Using this sex-specific information, we developed a simple PCR genotyping assay which accurately differentiates XY genetic males (amhr2by ) from XX genetic females (amhr2by ). Our high-quality genome assembly is an important genomic resource for future studies on yellow perch ecology, toxicology, fisheries and aquaculture research. In addition, characterization of the amhr2by gene as a candidate sex-determining gene in yellow perch provides a new example of the recurrent implication of the transforming growth factor beta pathway in fish sex determination, and highlights gene duplication as an important genomic mechanism for the emergence of new master sex determination genes.

  • Characterization of a Y-specific duplication/insertion of the Anti-Mullerian Hormone type II receptor gene based on a chromosome-scale genome assembly of yellow perch, Perca flavescens
    2019
    Co-Authors: Romain Feron, Margot Zahm, Cédric Cabau, Christophe Klopp, Céline Roques, Olivier Bouchez, Camille Eché, Sophie Valière, Cécile Donnadieu, Pierrick Haffray
    Abstract:

    Background: Yellow perch, Perca flavescens, is an ecologically and commercially important species native to a large portion of the northern United States and southern Canada. It is also a promising candidate species for aquaculture. No yellow perch reference genome, however, has been available to facilitate improvements in both fisheries and aquaculture management practices. Findings: By combining Oxford Nanopore Technologies long-reads, 10X genomics Illumina short linked reads and a chromosome contact map produced with Hi-C, we generated a high-continuity chromosome scale yellow perch genome assembly of 877.4 Mb. It contains, in agreement with the known diploid chromosome yellow perch count, 24 chromosome-size scaffolds covering 98.8% of the complete assembly (N50 = 37.4 Mb, L50 = 11). Genome annotation identified 41.7% (366 Mb) of repeated elements and 24,486 genes including 16,579 genes (76.3%) significantly matching with proteins in public databases. We also provide a first characterization of the yellow perch sex determination locus that contains a male-specific duplicate of the Anti-Mullerian Hormone type II receptor gene (amhr2by) inserted at the proximal end of the Y chromosome (chromosome 9). Using this sex-specific information, we developed a simple PCR genotyping test which accurately differentiates XY genetic males (amhr2by+) from XX genetic females (amhr2by−). Conclusions: Our high-quality genome assembly is an important genomic resource for future studies on yellow perch ecology, toxicology, fisheries, and aquaculture research. In addition, the characterization of the amhr2by gene as a candidate sex determining gene in yellow perch provides a new example of the recurrent implication of the transforming growth factor beta pathway in fish sex determination, and highlights gene duplication as an important genomic mechanism for the emergence of new master sex determination genes.

Luciano G. Nardo - One of the best experts on this subject based on the ideXlab platform.

Jenny A Visser - One of the best experts on this subject based on the ideXlab platform.

  • Fluctuations in anti-Müllerian Hormone levels throughout the menstrual cycle parallel fluctuations in the antral follicle count: a cohort study.
    Acta obstetricia et gynecologica Scandinavica, 2016
    Co-Authors: Martine Depmann, Jenny A Visser, Joop S E Laven, Jeroen Van Disseldorp, Simone L. Broer, Marinus J.c. Eijkemans, Yolanda B. De Rijke, Ben Willem J. Mol, Frank J.m. Broekmans
    Abstract:

    Introduction In this prospective cohort study we aimed to investigate the hypothesis that fluctuations in Anti-Mullerian Hormone levels stem from fluctuations in the number of antral follicles. Material and methods Repeated measurements of Anti-Mullerian Hormone and antral follicles (follicles 2–8 mm) were performed in 44 women with a regular cycle, during one menstrual cycle. If our hypothesis that Anti-Mullerian Hormone fluctuations stem from fluctuations in the antral follicles is correct, a fluctuation in the antral follicles would result in an equal and parallel shift in Anti-Mullerian Hormone. Hence, the difference between antral follicles and Anti-Mullerian Hormone would remain constant over time. A mixed model analysis, assessing the stability between Anti-Mullerian Hormone and antral follicles, was performed using the difference between logantral follicles and logAnti-Mullerian Hormone. Cohen's D was calculated for the largest of fixed effects in order to assess stability in relative distance between antral follicles and Anti-Mullerian Hormone. To assess if fluctuation in Anti-Mullerian Hormone or antral follicles originated from between-subject fluctuation, or from within subject fluctuation, the intra-class correlation coefficient was calculated. Results Mixed model analysis and Cohen's D (0.12) confirmed the stability of the difference between logantral follicles and logAnti-Mullerian Hormone and so confirmed our hypothesis. The good intra-class correlation coefficient (0.73) indicated a small contribution of within-subject variation to Anti-Mullerian Hormone fluctuations. Conclusions Fluctuations in Anti-Mullerian Hormone levels parallel fluctuations in antral follicles, suggesting that Anti-Mullerian Hormone levels are closely linked to variation in the antral follicles. This knowledge adds to the basic understanding of the origin of Anti-Mullerian Hormone and could aid in interpretation of individual Anti-Mullerian Hormone levels.

  • Anti-Müllerian Hormone in men with normal and reduced sperm concentration and men with maldescended testes.
    Fertility and sterility, 2008
    Co-Authors: Frank Tüttelmann, Axel P N Themmen, Jenny A Visser, Nina Dykstra, Eberhard Nieschlag, Manuela Simoni
    Abstract:

    Objective To evaluate serum Anti-Mullerian Hormone (AMH) in well-characterized men with normal and reduced sperm concentration and in men with a history of or persistent maldescended testes as a possible clinical marker of male factor infertility and/or maldescended testes. Design Retrospective analysis of 199 men selected from our database (Androbase). Setting The university-based Institute of Reproductive Medicine. Patient(s) One hundred eight men with normal and 60 men with reduced sperm concentration without known cause of infertility and additionally 31 infertile men with current or former maldescended testes were evaluated. Intervention(s) Serum AMH was analyzed by an in-house ELISA. Main Outcome Measure(s) Hormone and semen parameters were compared and correlated with AMH. Result(s) No significant differences were found in AMH levels. Only in men with maldescended testes did AMH correlate negatively with FSH and positively with testicular volume and sperm concentration. No correlations between AMH and LH or testosterone (T) were found. Conclusion(s) Anti-Mullerian Hormone serum levels are not significantly affected by impaired spermatogenesis in general but are correlated with spermatogenic parameters in men with current or former maldescended testes. Therefore, AMH measurement does not improve clinical routine diagnostics but should be evaluated further in patients with maldescended testes. Anti-Mullerian Hormone might serve as a marker of Sertoli cell number, function, and/or maturation in these men.

  • anti mullerian Hormone and anti mullerian Hormone type ii receptor polymorphisms are associated with follicular phase estradiol levels in normo ovulatory women
    Human Reproduction, 2007
    Co-Authors: Marlies E Kevenaar, Barbara Sonntag, Sharon Lie Fong, Manuela Simoni, Axel P N Themmen, Frank H. De Jong, Joop S E Laven, Huibert A P Pols, Andre G Uitterlinden, Jenny A Visser
    Abstract:

    textabstractBackground: In mice, Anti-Mullerian Hormone (AMH) inhibits primordial follicle recruitment and decreases FSH sensitivity. Little is known about the role of AMH in human ovarian physiology. We hypothesize that in women AMH has a similar role in ovarian function as in mice and investigated this using a genetic approach. Methods: The association ofthe AMH Ile49Ser and the AMH type II receptor (AMHR2) -482 A > G polymorphisms with menstrual cycle characteristics was studied in a Dutch (n = 32) and a German (n = 21) cohort of normo-ovulatory women. Results: Carriers of the AMH Ser49allele had higher serum estradiol (E2) levels on menstrual cycle day 3 when compared with non-carriers in the Dutch cohort (P = 0.012) and in the combined Dutch and German cohort (P = 0.03). Carriers of the AMHR2 -482G allele also had higher follicular phase E2levels when compared with non-carriers in the Dutch cohort (P = 0.028), the German cohort (P = 0.048) and hence also the combined cohort (P = 0.012). Women carrying both AMH Ser49and AMHR2 -482G alleles had highest E2levels (P = 0.001). For both polymorphisms no association with serum AMH or FSH levels was observed. Conclusions: Polymorphisms in the AMH and AMHR2 genes are associated with follicular phase E2levels, suggesting a role for AMH in the regulation of FSH sensitivity in the human ovary.