Dr Diane Rebourcet
Honorary Lecturer
School of Environmental and Life Sciences
- Email:diane.rebourcet@newcastle.edu.au
- Phone:(02)491 38060
Career Summary
Biography
After attending fascinating lectures in Life Sciences, while undertaking my undergraduate studies at Paris-Denis-Diderot University, France, I decided to specialise in Reproduction and Development and completed a Masters degree in that same institution. I then began a PhD focussing on the impact of environmental endocrine disruptors on the reproductive system at Lyon-Claude-Bernard University, France. In 2011, thanks to a fellowship from the Servier Institute (a non-profit association), I obtained funding to pursue my postdoctoral studies at the University of Edinburgh in the Centre for Reproductive Health, and in 2018, I was recruited by the University of Newcastle as a Postdoctoral Research Associate.
Research expertise
My work includes a variety of subjects that reflect my research interests from when I first graduated to present day. From an early start in biological sciences, I carried out research in the area of reproduction, mainly focusing on reproductive pathologies and starting with the female reproductive system in relation with ovarian disorders (PCOS and premature ovarian failure). During my postgraduate studies, I felt especially pertained by the impact and consequences of the environment on human health, and therefore, extended my research interests to reproductive toxicology and endocrine disruption. Undertaking my PhD and first postdoctoral position in this field, I had the opportunity to address the impact of endocrine disruption on the male reproductive system development and function. My current research focuses on understanding the mechanisms and regulations affecting the reproductive system, amongst which the androgen biosynthesis (mainly undertaken by the Leydig cells) and in developing new approaches for potential therapies to benefit male health.
Current aspects of research:
- The recent identification of new roles for Sertoli cells has fundamentally changed our understanding of testis biology regarding its development and function. My research interest is to pursue the characterisation of Sertoli cell roles and to utilise their properties as biological therapeutical tools.
- Demonstrating the complexity of Sertoli cell regulation of Leydig cell development and function, Sertoli cells appear as a novel target for endocrine disruption and/or potential therapy to improve androgen profile. One focus on my ongoing research is to identify Sertoli cell factors that can regulate Leydig cells function,
- With the recent identification of differential androgens pathways (classical and backdoor), another aspect of my ongoing research focuses on deciphering the importance of both classical and backdoor androgen pathways on testis development and function.
- With a better understanding of androgen regulation, finding targeted and suitable therapies is another topic of my current research.
Common approaches: transgenic mouse models, “gene therapy”, biotechnologies, in silico modelling as well as usual bio-molecular techniques.
Teaching expertise
I have lectured for the University of Edinburgh in the Reproductive Systems (BIME10016) Undergraduate 4th year Course since 2014. I had the opportunity during my position in Edinburgh to be involved in the day-to-day supervision of PhD students and to supervise laboratory projects for both Bachelor of Science (Reproductive Biology) and Master of Science (Reproductive Science) students, both of which graduated with distinction.
Collaborations
I am working in close collaboration with world leading researchers: Peter O’Shaughnessy (University of Glasgow), Rod Mitchell (University of Edinburgh), Serge Nef (University of Geneva), Peter Stanton and Liza O’Donnell (Hudson Institute of Medical Research).
If you are a prospective Honours/PhD student and interested in joining the laboratory, please contact me via email: diane.rebourcet@newcastle.edu.au
Qualifications
- PhD (Reproductive Biology), Claude Bernard University Lyon 1, France
- Master in Cellular Biology Physiology & Pathology, Claude Bernard University Lyon 1, France
Keywords
- Biotechnology
- Endocrine disruptors
- Endocrinology
- Fertility
- Gene therapy
- Infertility
- Reproductive Biology
- Reproductive Sciences
Languages
- French (Mother)
- English (Fluent)
Fields of Research
Code | Description | Percentage |
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320208 | Endocrinology | 40 |
310903 | Animal developmental and reproductive biology | 45 |
310999 | Zoology not elsewhere classified | 15 |
Professional Experience
Academic appointment
Dates | Title | Organisation / Department |
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17/6/2015 - 31/3/2018 | Postdoctoral Research fellow | University of Edinburgh Medical Research Council (MRC) Centre for Reproductive Health United Kingdom |
15/6/2011 - 17/6/2012 | Post-doctorate researcher | University of Edinburgh Medical Research Council (MRC) Centre for Reproductive Health United Kingdom |
Invitations
Keynote Speaker
Year | Title / Rationale |
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2018 | Effect of Sertoli cell ablation on testicular development and function. |
Publications
For publications that are currently unpublished or in-press, details are shown in italics.
Chapter (1 outputs)
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2018 |
Rebourcet D, Darbey A, Curley M, O Shaughnessy P, Smith LB, 'Testicular cell selective ablation using diphtheria toxin receptor transgenic mice', Sertoli Cells: Methods and Protocols, Humana Press, New York, NY 203-228 (2018) [B1]
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Journal article (33 outputs)
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2023 |
Fraser BA, Wilkins AL, De Iuliis GN, Rebourcet D, Nixon B, Aitken RJ, 'Development of a model for studying the developmental consequences of oxidative sperm DNA damage by targeting redox-cycling naphthoquinones to the Sertoli cell population.', Free radical biology & medicine, 206 50-62 (2023) [C1]
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2023 |
O Donnell L, Dagley LF, Curley M, Darbey A, O Shaughnessy PJ, Diemer T, et al., 'Sertoli cell-enriched proteins in mouse and human testicular interstitial fluid', PLoS ONE, 18 (2023) [C1] Sertoli cells support the development of sperm and the function of various somatic cells in the interstitium between the tubules. Sertoli cells regulate the function of the testic... [more] Sertoli cells support the development of sperm and the function of various somatic cells in the interstitium between the tubules. Sertoli cells regulate the function of the testicular vasculature and the development and function of the Leydig cells that produce testosterone for fertility and virility. However, the Sertoli cell-derived factors that regulate these cells are largely unknown. To define potential mechanisms by which Sertoli cells could support testicular somatic cell function, we aimed to identify Sertoli cell-enriched proteins in the testicular interstitial fluid (TIF) between the tubules. We previously resolved the proteome of TIF in mice and humans and have shown it to be a rich source of seminiferous tubule-derived proteins. In the current study, we designed bioinformatic strategies to interrogate relevant proteomic and genomic datasets to identify Sertoli cell-enriched proteins in mouse and human TIF. We analysed proteins in mouse TIF that were significantly reduced after one week of acute Sertoli cell ablation in vivo and validated which of these are likely to arise primarily from Sertoli cells based on relevant mouse testis RNASeq datasets. We used a different, but complementary, approach to identify Sertoli cell-enriched proteins in human TIF, taking advantage of high-quality human testis genomic, proteomic and immunohistochemical datasets. We identified a total of 47 and 40 Sertoli cell-enriched proteins in mouse and human TIF, respectively, including 15 proteins that are conserved in both species. Proteins with potential roles in angiogenesis, the regulation of Leydig cells or steroidogenesis, and immune cell regulation were identified. The data suggests that some of these proteins are secreted, but that Sertoli cells also deposit specific proteins into TIF via the release of extracellular vesicles. In conclusion, we have identified novel Sertoli cell-enriched proteins in TIF that are candidates for regulating somatic cell-cell communication and testis function.
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2022 |
Curley M, Darbey A, O'Donnell L, Kilcoyne KR, Wilson K, Mungall W, et al., 'Leukemia inhibitory factor-receptor signalling negatively regulates gonadotrophin-stimulated testosterone production in mouse Leydig Cells: LIFR Signalling in Leydig Cells', Molecular and Cellular Endocrinology, 544 (2022) [C1] Testicular Leydig cells (LCs) are the principal source of circulating testosterone in males. LC steroidogenesis maintains sexual function, fertility and general health, and is inf... [more] Testicular Leydig cells (LCs) are the principal source of circulating testosterone in males. LC steroidogenesis maintains sexual function, fertility and general health, and is influenced by various paracrine factors. The leukemia inhibitory factor receptor (LIFR) is expressed in the testis and activated by different ligands, including leukemia inhibitory factor (LIF), produced by peritubular myoid cells. LIF can modulate LC testosterone production in vitro under certain circumstances, but the role of consolidated signalling through LIFR in adult LC function in vivo has not been established. We used a conditional Lifr allele in combination with adenoviral vectors expressing Cre-recombinase to generate an acute model of LC Lifr-KO in the adult mouse testis, and showed that LC Lifr is not required for short term LC survival or basal steroidogenesis. However, LIFR-signalling negatively regulates steroidogenic enzyme expression and maximal gonadotrophin-stimulated testosterone biosynthesis, expanding our understanding of the intricate regulation of LC steroidogenic function.
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2022 |
Shaw IWW, Kirkwood PMM, Rebourcet D, Cousins FLL, Ainslie RJJ, Livingstone DEW, et al., 'A role for steroid 5 alpha-reductase 1 in vascular remodeling during endometrial decidualization', FRONTIERS IN ENDOCRINOLOGY, 13 (2022) [C1]
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2022 |
Gannon A-L, Darbey ALL, Chensee G, Lawrence BMM, O'Donnell L, Kelso J, et al., 'A Novel Model Using AAV9-Cre to Knockout Adult Leydig Cell Gene Expression Reveals a Physiological Role of Glucocorticoid Receptor Signalling in Leydig Cell Function', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 23 (2022) [C1]
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2022 |
O'Donnell L, Smith LB, Rebourcet D, 'Sertoli cells as key drivers of testis function', Seminars in Cell and Developmental Biology, 121 2-9 (2022) [C1] Sertoli cells are the orchestrators of spermatogenesis; they support fetal germ cell commitment to the male pathway and are essential for germ cell development, from maintenance o... [more] Sertoli cells are the orchestrators of spermatogenesis; they support fetal germ cell commitment to the male pathway and are essential for germ cell development, from maintenance of the spermatogonial stem cell niche and spermatogonial populations, through meiosis and spermiogeneis and to the final release of mature spermatids during spermiation. However, Sertoli cells are also emerging as key regulators of other testis somatic cells, including supporting peritubular myoid cell development in the pre-pubertal testis and supporting the function of the testicular vasculature and in contributing to testicular immune privilege. Sertoli cells also have a major role in regulating androgen production within the testis, by specifying interstitial cells to a steroidogenic fate, contributing to androgen production in the fetal testis, and supporting fetal and adult Leydig cell development and function. Here, we provide an overview of the specific roles for Sertoli cells in the testis and highlight how these cells are key drivers of testicular sperm output, and of adult testis size and optimal function of other testicular somatic cells, including the steroidogenic Leydig cells.
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2022 |
O'Donnell L, Smith LB, Rebourcet D, 'Sperm-specific proteins: new implications for diagnostic development and cancer immunotherapy.', Curr Opin Cell Biol, 77 102104 (2022) [C1]
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2022 |
Lawrence BM, O'Donnell L, Smith LB, Rebourcet D, 'New Insights into Testosterone Biosynthesis: Novel Observations from HSD17B3 Deficient Mice.', International journal of molecular sciences, 23 15555 (2022) [C1]
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2021 |
O'Donnell L, Rebourcet D, Dagley LF, Sgaier R, Infusini G, O'Shaughnessy PJ, et al., 'Sperm proteins and cancer-testis antigens are released by the seminiferous tubules in mice and men', FASEB Journal, 35 (2021) [C1] Sperm develop from puberty in the seminiferous tubules, inside the blood-testis barrier to prevent their recognition as ¿non-self¿ by the immune system, and it is widely assumed t... [more] Sperm develop from puberty in the seminiferous tubules, inside the blood-testis barrier to prevent their recognition as ¿non-self¿ by the immune system, and it is widely assumed that human sperm-specific proteins cannot access the circulatory or immune systems. Sperm-specific proteins aberrantly expressed in cancer, known as cancer-testis antigens (CTAs), are often pursued as cancer biomarkers and therapeutic targets based on the assumption they are neoantigens absent from the circulation in healthy men. Here, we identify a wide range of germ cell-derived and sperm-specific proteins, including multiple CTAs, that are selectively deposited by the Sertoli cells of the adult mouse and human seminiferous tubules into testicular interstitial fluid (TIF) that is ¿outside¿ the blood-testis barrier. From TIF, the proteins can access the circulatory- and immune systems. Disruption of spermatogenesis decreases the abundance of these proteins in mouse TIF, and a sperm-specific CTA is significantly decreased in TIF from infertile men, suggesting that exposure of certain CTAs to the immune system could depend on fertility status. The results provide a rationale for the development of blood-based tests useful in the management of male infertility and indicate CTA candidates for cancer immunotherapy and biomarker development that could show sex-specific and male-fertility-related responses.
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2021 |
Fraser B, Peters AE, Sutherland JM, Liang M, Rebourcet D, Nixon B, Aitken RJ, 'Biocompatible Nanomaterials as an Emerging Technology in Reproductive Health; a Focus on the Male', Frontiers in Physiology, 12 (2021) [C1] A growing body of research has confirmed that nanoparticle (NP) systems can enhance delivery of therapeutic and imaging agents as well as prevent potentially damaging systemic exp... [more] A growing body of research has confirmed that nanoparticle (NP) systems can enhance delivery of therapeutic and imaging agents as well as prevent potentially damaging systemic exposure to these agents by modifying the kinetics of their release. With a wide choice of NP materials possessing different properties and surface modification options with unique targeting agents, bespoke nanosystems have been developed for applications varying from cancer therapeutics and genetic modification to cell imaging. Although there remain many challenges for the clinical application of nanoparticles, including toxicity within the reproductive system, some of these may be overcome with the recent development of biodegradable nanoparticles that offer increased biocompatibility. In recognition of this potential, this review seeks to present recent NP research with a focus on the exciting possibilities posed by the application of biocompatible nanomaterials within the fields of male reproductive medicine, health, and research.
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2021 |
Darbey A, Rebourcet D, Curley M, Kilcoyne K, Jeffery N, Reed N, et al., 'A comparison of in vivo viral targeting systems identifies adeno-associated virus serotype 9 (AAV9) as an effective vector for genetic manipulation of Leydig cells in adult mice', ANDROLOGY, 9 460-473 (2021) [C1]
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2021 |
Sararols P, Stevant I, Neirijnck Y, Rebourcet D, Darbey A, Curley MK, et al., 'Specific Transcriptomic Signatures and Dual Regulation of Steroidogenesis Between Fetal and Adult Mouse Leydig Cells', FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY, 9 (2021) [C1]
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2020 |
Rebourcet D, Mackay R, Darbey A, Curley MK, Jørgensen A, Frederiksen H, et al., 'Ablation of the canonical testosterone production pathway via knockout of the steroidogenic enzyme HSD17B3, reveals a novel mechanism of testicular testosterone production', FASEB Journal, 34 10373-10386 (2020) [C1]
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2019 |
Rebourcet D, Monteiro A, Cruickshanks L, Jeffery N, Smith S, Milne L, et al., 'Relationship of transcriptional markers to Leydig cell number in the mouse testis', PloS one, 14 (2019) [C1]
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2019 |
Gannon A-L, O'Hara L, Mason JI, Rebourcet D, Smith S, Traveres A, et al., 'Ablation of glucocorticoid receptor in the hindbrain of the mouse provides a novel model to investigate stress disorders', SCIENTIFIC REPORTS, 9 (2019) [C1]
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2019 |
Rebourcet D, O'Shaughnessy PJ, Smith LB, 'The expanded roles of Sertoli cells: lessons from Sertoli cell ablation models', Current Opinion in Endocrine and Metabolic Research, 6 42-48 (2019) [C1]
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2018 |
Curley M, Milne L, Smith S, Atanassova N, Rebourcet D, Darbey A, et al., 'Leukemia Inhibitory Factor-Receptor is Dispensable for Prenatal Testis Development but is Required in Sertoli cells for Normal Spermatogenesis in Mice', SCIENTIFIC REPORTS, 8 (2018) [C1]
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2017 |
van den Driesche S, Kilcoyne KR, Wagner I, Rebourcet D, Boyle A, Mitchell R, et al., 'Experimentally induced testicular dysgenesis syndrome originates in the masculinization programming window', JCI Insight, 2 (2017) The testicular dysgenesis syndrome (TDS) hypothesis, which proposes that common reproductive disorders of newborn and adult human males may have a common fetal origin, is largely ... [more] The testicular dysgenesis syndrome (TDS) hypothesis, which proposes that common reproductive disorders of newborn and adult human males may have a common fetal origin, is largely untested. We tested this hypothesis using a rat model involving gestational exposure to dibutyl phthalate (DBP), which suppresses testosterone production by the fetal testis. We evaluated if induction of TDS via testosterone suppression is restricted to the ¿masculinization programming window¿ (MPW), as indicated by reduction in anogenital distance (AGD). We show that DBP suppresses fetal testosterone equally during and after the MPW, but only DBP exposure in the MPW causes reduced AGD, focal testicular dysgenesis, and TDS disorders (cryptorchidism, hypospadias, reduced adult testis size, and compensated adult Leydig cell failure). Focal testicular dysgenesis, reduced size of adult male reproductive organs, and TDS disorders and their severity were all strongly associated with reduced AGD. We related our findings to human TDS cases by demonstrating similar focal dysgenetic changes in testes of men with preinvasive germ cell neoplasia (GCNIS) and in testes of DBP-MPW animals. If our results are translatable to humans, they suggest that identification of potential causes of human TDS disorders should focus on exposures during a human MPW equivalent, especially if negatively associated with offspring AGD.
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2017 |
Soffientini U, Rebourcet D, Abel MH, Lee S, Hamilton G, Fowler PA, et al., 'Identification of Sertoli cell-specific transcripts in the mouse testis and the role of FSH and androgen in the control of Sertoli cell activity', BMC GENOMICS, 18 (2017) [C1]
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2017 |
Rebourcet D, Darbey A, Monteiro A, Soffientini U, Tsai YT, Handel I, et al., 'Sertoli Cell Number Defines and Predicts Germ and Leydig Cell Population Sizes in the Adult Mouse Testis', ENDOCRINOLOGY, 158 2955-2969 (2017) [C1]
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2017 |
Patel SH, O'Hara L, Atanassova N, Smith SE, Curley MK, Rebourcet D, et al., 'Low-dose tamoxifen treatment in juvenile males has long-term adverse effects on the reproductive system: implications for inducible transgenics.', Scientific Reports, 7 (2017) [C1]
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2015 |
Guillermet-Guibert J, Smith LB, Halet G, Whitehead MA, Pearce W, Rebourcet D, et al., 'Novel Role for p110 beta PI 3-Kinase in Male Fertility through Regulation of Androgen Receptor Activity in Sertoli Cells', PLOS GENETICS, 11 (2015) [C1]
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2015 |
Smith LB, O'Shaughnessy PJ, Rebourcet D, 'Cell-specific ablation in the testis: what have we learned?', ANDROLOGY, 3 1035-1049 (2015) [C1]
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2014 |
Rebourcet D, O'Shaughnessy PJ, Pitetti J-L, Monteiro A, O'Hara L, Milne L, et al., 'Sertoli cells control peritubular myoid cell fate and support adult Leydig cell development in the prepubertal testis', DEVELOPMENT, 141 2139-2149 (2014) [C1]
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2014 |
Rebourcet D, O'Shaughnessy PJ, Monteiro A, Milne L, Cruickshanks L, Jeffrey N, et al., 'Sertoli Cells Maintain Leydig Cell Number and Peritubular Myoid Cell Activity in the Adult Mouse Testis', PLOS ONE, 9 (2014) [C1]
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2013 | Halperin J, Devi YS, Elizur S, Stocco C, Shehu A, Rebourcet D, et al., 'Prolactin Signaling through the Short Form of Its Receptor Represses Forkhead Transcription Factor FOXO3 and Its Target Gene galt Causing a Severe Ovarian Defect (vol 22, pg 513, 2008)', MOLECULAR ENDOCRINOLOGY, 27 1981-1981 (2013) | ||||||||||
2012 |
Magre S, Rebourcet D, Ishaq M, Wargnier R, Debard C, Meugnier E, et al., 'Gender differences in transcriptional signature of developing rat testes and ovaries following embryonic exposure to 2,3,7,8-TCDD', PLoS ONE, 7 (2012) Dioxins are persistent organic pollutants interfering with endocrine systems and causing reproductive and developmental disorders. The objective of our project was to determine th... [more] Dioxins are persistent organic pollutants interfering with endocrine systems and causing reproductive and developmental disorders. The objective of our project was to determine the impact of an in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on reproductive function of male and female offspring in the rat with a special emphasis on the immature period. We used a low dose of TCDD (unique exposure by oral gavage of 200 ng/kg at 15.5 days of gestation) in order to mirror a response to an environmental dose of TCDD not altering fertility of the progeny. We choose a global gene expression approach using Affymetrix microarray analysis, and testes of 5 days and ovaries of 14 days of age. Less than 1% of the expressed genes in gonads were altered following embryonic TCDD exposure; specifically, 113 genes in ovaries and 56 in testes with 7 genes common to both sex gonads. It included the repressor of the aryl hydrocarbon receptor (Ahrr), the chemokines Ccl5 and Cxcl4 previously shown to be regulated by dioxin in testis, Pgds2/Hpgds and 3 others uncharacterized. To validate and extend the microarray data we realized real-time PCR on gonads at various developmental periods of interest (from 3 to 25 days for ovaries, from 5 to the adult age for testes). Overall, our results evidenced that both sex gonads responded differently to TCDD exposure. For example, we observed induction of the canonic battery of TCDD-induced genes coding enzymes of the detoxifying machinery in ovaries aged of 3-14 days of age (except Cyp1a1 induced at 3-10 days) but not in testes of 5 days (except Ahrr). We also illustrated that inflammatory pathway is one pathway activated by TCDD in gonads. Finally, we identified several new genes targeted by TCDD including Fgf13 in testis and one gene, Ptgds2/Hpgds regulated in the two sex gonads. © 2012 Magre et al.
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2011 |
Naville D, Rebourcet D, Chauvin MA, Vega N, Jalabert A, Vigier M, et al., 'Direct and indirect impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on adult mouse Leydig cells: An in vitro study', Toxicology Letters, 207 251-257 (2011) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related substances are ubiquitous environmental pollutants that exert adverse effects on reproductive processes. In testis, Leydig c... [more] 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related substances are ubiquitous environmental pollutants that exert adverse effects on reproductive processes. In testis, Leydig cells which produce testosterone are under hormonal and local control exerted by cytokines including TNFa. Using mouse Leydig primary cell cultures as a model, we studied the effects of TCDD on the steroidogenic outcome of Leydig cells and the gene expression levels of Ccl5 and Cxcl4, previously shown to be target genes of TCDD in testis. We found that TCDD did not alter the steroidogenic outcome of Leydig cells but that it up-regulated Cxcl4 gene expression levels. TCDD also impacted Ccl5 gene expression when cells had been co-treated with TNFa. TCDD action probably initiated with binding to the aryl hydrocarbon receptor (AhR) present on Leydig cells. TCDD regulated the gene expression levels of AhR (transient down-regulation) and its repressor AhRR and Cyp1b1 (up-regulation). The trophic human chorionic gonadotropin (hCG) hormone did not impact AhR, its repressor AhRR or Cyp1b1 but it opposed the TCDD-enhanced AhRR mRNA levels. Conversely, TNFa stimulated AhR gene expression levels. Collectively, it is suggested that the impact of TCDD on expression of target genes in Leydig cells may operate under the complex network of hormones and cytokines. © 2011 Elsevier Ireland Ltd.
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2010 |
Rebourcet D, Odet F, Vérot A, Combe E, Meugnier E, Pesenti S, et al., 'The effects of an in utero exposure to 2,3,7,8-tetrachloro-dibenzo-p-dioxin on male reproductive function: Identification of Ccl5 as a potential marker', International Journal of Andrology, 33 413-424 (2010) 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dioxin-like compounds are widely encountered toxic substances suspected of interfering with the endocrine systems of humans and wild... [more] 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and dioxin-like compounds are widely encountered toxic substances suspected of interfering with the endocrine systems of humans and wildlife, and of contributing to the loss of fertility. In this study, we determined the changes in testicular gene expression caused by in utero exposure to TCDD along with the intra-testicular testosterone levels, epididymal sperm reserves, daily sperm production (DSP) and testis histology. To this purpose, female pregnant Sprague-Dawley rats orally received TCDD (10, 100 or 200 ng/kg body weight) or vehicle at embryonic day 15, and the offspring was killed throughout development. Hepatic Cyp1a1 gene expression was measured in the offspring to confirm the exposure to TCDD. The gross histology of the testes and intra-testicular testosterone levels were normal among the studied groups. Sperm reserves were altered in 67-day-old rats of the TCDD-200 group, but not in 145-day-old animals or in the other TCDD-exposed groups. Nonetheless, fertility was not altered in males of the TCDD-200 group, and the F2 males generated had normal sperm reserves and DSP. Microarray analysis permitted the identification of eight differentially expressed genes in the 4-week-old testes of the TCDD-200 compared with that of the control group (cut-off value ± 1.40), including the down-regulated chemokine Ccl5/Rantes. Inhibition of Ccl5/Rantes gene expression was observed throughout development in the TCDD-200 group, and at 67 and 145 days in the TCDD-100 group (animals of younger ages were not examined). Ccl5/Rantes gene expression was mostly confined in Leydig cells. F2 males generated from males of the TCDD-200 group had normal levels of Ccl5/Rantes in testis and Cyp1a1 in liver, which might indicate that Ccl5/Rantes is a marker of TCDD exposure in testis such as Cyp1a1 in liver. In conclusion, we demonstrated a decrease in Ccl5/Rantes RNA levels and a transitory decline in sperm reserves in the testes of rats of TCDD-dosed dams. © 2010 European Academy of Andrology.
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2010 |
Bachelot A, Bouilly J, Liu Y, Rebourcet D, Leux C, Kuttenn F, et al., 'Sequence variation analysis of the prolactin receptor C-terminal region in women with premature ovarian failure', FERTILITY AND STERILITY, 94 2772-2775 (2010)
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2008 |
Halperin J, Devi SY, Elizur S, Stocco C, Shehu A, Rebourcet D, et al., 'Prolactin signaling through the short form of its receptor represses forkhead transcription factor FOXO3 and its target gene galt causing a severe ovarian defect', MOLECULAR ENDOCRINOLOGY, 22 513-522 (2008)
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Show 30 more journal articles |
Conference (3 outputs)
Year | Citation | Altmetrics | Link | ||
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2014 | van den Driesche S, Rebourcet D, Kilcoyne K, Sharpe RM, 'Fetal Androgen Suppression in the Masculinisation Programming Window (MPW) Determines Adult Reproductive Disorders in the Rat', ENDOCRINE REVIEWS (2014) | ||||
2011 |
Naville D, Rebourcet D, Chauvin M, Vega N, Jalabert A, Vigier M, et al., 'Impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult mouse Leydig cells: An in vitro study', TOXICOLOGY LETTERS, Paris, FRANCE (2011)
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2011 |
Magre S, Rebourcet D, Ishaq M, Wargnier R, Debard C, Vidal H, et al., 'Alterations in the transcriptome of the developing ovaries and testes following embryonic exposure to 2,3,7,8-TCDD', TOXICOLOGY LETTERS, Paris, FRANCE (2011)
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Preprint (2 outputs)
Year | Citation | Altmetrics | Link | |||||
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2022 |
Shaw IW, Kirkwood PM, Rebourcet D, Cousins FL, Ainslie RJ, Livingstone DEW, et al., 'A Role for Steroid 5 alpha-reductase 1 in Vascular Remodelling During Endometrial Decidualisation (2022)
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2021 |
Sararols P, Stévant I, Neirijnck Y, Rebourcet D, Darbey A, Curley M, et al., 'Specific transcriptomic signatures and dual regulation of steroidogenesis between fetal and adult mouse Leydig cells (2021)
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Grants and Funding
Summary
Number of grants | 11 |
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Total funding | $843,091 |
Click on a grant title below to expand the full details for that specific grant.
20222 grants / $190,612
MRSP transition funding – Pregnancy and Reproduction program$185,612
Funding body: Hunter Medical Resarch Institute (HMRI) Public Health Program
Funding body | Hunter Medical Resarch Institute (HMRI) Public Health Program |
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Scheme | program grant |
Role | Investigator |
Funding Start | 2022 |
Funding Finish | 2023 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
CESE faculty funding- Development of a novel inducible model of androgen deficiency$5,000
Funding body: College of Engineering, Science and Environment (CESE), University of Newcastle
Funding body | College of Engineering, Science and Environment (CESE), University of Newcastle |
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Scheme | CESE faculty funding |
Role | Lead |
Funding Start | 2022 |
Funding Finish | 2022 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20212 grants / $38,000
Defining the role of glucocorticoids in testis function and fertility$28,000
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
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Project Team | Doctor Diane Rebourcet, Doctor Anne-Louise Gannon |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2021 |
Funding Finish | 2022 |
GNo | G2101102 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
A pioneering approach to switch on/off steroid production using light.$10,000
Funding body: Endocrine Society of Australia
Funding body | Endocrine Society of Australia |
---|---|
Project Team | Doctor Diane Rebourcet |
Scheme | Seed Funding |
Role | Lead |
Funding Start | 2021 |
Funding Finish | 2022 |
GNo | G2101119 |
Type Of Funding | C3200 – Aust Not-for Profit |
Category | 3200 |
UON | Y |
20192 grants / $541,185
The Importance of Classical Versus Backdoor Androgen Production Pathways in Masculinisation, Fertility and Lifelong Male Health$521,327
Funding body: NHMRC (National Health & Medical Research Council)
Funding body | NHMRC (National Health & Medical Research Council) |
---|---|
Project Team | Professor Lee Smith, Doctor Diane Rebourcet |
Scheme | Project Grant |
Role | Investigator |
Funding Start | 2019 |
Funding Finish | 2021 |
GNo | G1800098 |
Type Of Funding | C1100 - Aust Competitive - NHMRC |
Category | 1100 |
UON | Y |
Investigating the regulation of androgen production to support healthy male ageing across the life course$19,858
Funding body: Hunter Medical Research Institute
Funding body | Hunter Medical Research Institute |
---|---|
Project Team | Doctor Diane Rebourcet, Doctor Elizabeth Bromfield, Dr Curley Michael |
Scheme | Research Grant |
Role | Lead |
Funding Start | 2019 |
Funding Finish | 2022 |
GNo | G1901563 |
Type Of Funding | C3300 – Aust Philanthropy |
Category | 3300 |
UON | Y |
20161 grants / $1,000
Society For Endocrinology travel grant $1,000
Funding body: Society For Endocrinology
Funding body | Society For Endocrinology |
---|---|
Project Team | Dr Diane Rebourcet |
Scheme | SFE-Travel grant |
Role | Lead |
Funding Start | 2016 |
Funding Finish | 2016 |
GNo | |
Type Of Funding | External |
Category | EXTE |
UON | N |
20151 grants / $18,000
Determining the Testicular Interstitial Fluid Proteome: Identification of Sertoli cell-derived paracrine factors regulating lifelong Leydig cell function.$18,000
Funding body: Society For Endocrinology
Funding body | Society For Endocrinology |
---|---|
Project Team | Dr Diane Rebourcet (CIA), Prof Lee Smith, Dr Peter Stanton, Dr Liza O'Donnell |
Scheme | SFE-Early Career Grant |
Role | Lead |
Funding Start | 2015 |
Funding Finish | 2015 |
GNo | |
Type Of Funding | External |
Category | EXTE |
UON | N |
20121 grants / $3,614
MSc Reproductive Science studentship, University of Edinburgh.$3,614
Funding body: MSc Reproductive Science studentship
Funding body | MSc Reproductive Science studentship |
---|---|
Project Team | Dr Diane Rebourcet (PI), Annalucia Darbey (student) |
Scheme | MSc Reproductive Science studentship, University of Edinburgh. |
Role | Lead |
Funding Start | 2012 |
Funding Finish | 2013 |
GNo | |
Type Of Funding | Internal |
Category | INTE |
UON | N |
20111 grants / $31,680
Timing and regulation of Sertoli cell proliferation in perinatal life and its vulnerability to disruption by lifestyle/environmental chemical exposures.$31,680
Funding body: Research funding from Servier Association
Funding body | Research funding from Servier Association |
---|---|
Project Team | Dr Diane Rebourcet (CIA), Pr Richard Sharpe |
Scheme | Research funding |
Role | Lead |
Funding Start | 2011 |
Funding Finish | 2012 |
GNo | |
Type Of Funding | External |
Category | EXTE |
UON | N |
20101 grants / $19,000
Effects of an in Utero Exposure to 2,3-7,8 TCDD on the rat reproductive system and role of the aryl hydrocarbon receptor in mouse testicular physiology.$19,000
Funding body: Schering-Plough research funds
Funding body | Schering-Plough research funds |
---|---|
Project Team | Diane Rebourcet (CIA), Dr Brigitte Battistoni-Le Magueresse |
Scheme | Research funds |
Role | Investigator |
Funding Start | 2010 |
Funding Finish | 2010 |
GNo | |
Type Of Funding | External |
Category | EXTE |
UON | N |
Dr Diane Rebourcet
Position
Honorary Lecturer
Lee Smith Group
School of Environmental and Life Sciences
College of Engineering, Science and Environment
Contact Details
diane.rebourcet@newcastle.edu.au | |
Phone | (02)491 38060 |
Fax | (02) 49216308 |
Office
Room | Life Sciences Building - LS2.02 |
---|---|
Building | Life Sciences Building |
Location | Callaghan University Drive Callaghan, NSW 2308 Australia |