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1,306 results on '"McNeilly, A. S."'

4. Evolutionary survival strategies of the female giant panda: optimizing energy resources and expenditure prior to pregnancy by postponing corpus luteum reactivation

Author

Wauters, Jella Rene M, primary, Wilson, Kirsten S, additional, Bouts, Tim, additional, Vancsok, Catherine, additional, Mulot, Baptiste, additional, Leclerc, Antoine, additional, Haapakoski, Marko, additional, Kok, Jose, additional, Kuehne, Ragnar, additional, Ochs, Andreas, additional, McNeilly, Alan S, additional, Rae, Mick, additional, Andrew, Ruth, additional, Duncan, W. Colin, additional, Girling, Simon J, additional, Zhou, Quang, additional, Li, Rengui, additional, Zhou, Yingmin, additional, Cai, Kailai, additional, Liu, Yuliang, additional, Hou, Rong, additional, Valentine, Iain, additional, Hildebrandt, Thomas B, additional, Li, Desheng, additional, and Vanhaecke, Lynn, additional

Published
2022
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20. The orphan nuclear receptor small heterodimer partner mediates male infertility induced by diethylstilbestrol in mice

Author

Volle, David H., Decourteix, Melanie, Garo, Erwan, McNeilly, Judy, Fenichel, Patrick, Auwerx, Johan, McNeilly, Alan S., Schoonjans, Kristina, and Benahmed, Mohamed

Subjects
Infertility -- Genetic aspects, Phenols, Diethylstilbestrol, Testosterone -- Genetic aspects, Health care industry
Abstract

Studies in rodents have shown that male sexual function can be disrupted by fetal or neonatal administration of compounds that alter endocrine homeostasis, such as the synthetic nonsteroidal estrogen diethylstilbestrol (DES). Although the molecular basis for this effect remains unknown, estrogen receptors likely play a critical role in mediating DES-induced infertility. Recently, we showed that the orphan nuclear receptor small heterodimer partner (Nr0b2), which is both a target gene and a transcriptional repressor of estrogen receptors, controls testicular function by regulating germ cell entry into meiosis and testosterone synthesis. We therefore hypothesized that some of the harmful effects of DES on testes could be mediated through Nr0b2. Here, we present data demonstrating that Nr0b2 deficiency protected mice against the negative effects of DES on testis development and function. During postnatal development, Nr0b2-null mice were resistant to DES-mediated inhibition of germ cell differentiation, which maybe the result of interference by Nr0b2 with retinoid signals that control meiosis. Adult Nr0b2-null male mice were also protected against the effects of DES; however, we suggest that this phenomenon was due to the removal of the repressive effects of Nr0b2 on steroidogenesis. Together, these data demonstrate that Nr0b2 plays a critical role in the pathophysiological changes induced by DES in the mouse testis., Introduction The small heterodimer partner (Shp; referred to herein as Nr0b2) is mainly known for its role in the liver, where it is involved in the feedback inhibition of bile [...]

Published
2009
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22. Gonadotrope and thyrotrope development in the human and mouse anterior pituitary gland

Author

Pope, Caroline, McNeilly, Judy R., Coutts, Shiona, Millar, Mike, Anderson, Richard A., and McNeilly, Alan S.

Subjects
Gonadotropin -- Analysis, Gene expression -- Analysis, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.05.005 Byline: Caroline Pope, Judy R. McNeilly, Shiona Coutts, Mike Millar, Richard A. Anderson, Alan S. McNeilly Keywords: Developmental changes; Hormonal identity; Human fetal pituitary; Mouse embryonic pituitary; Gonadotrope lineage; Thyrotrope lineage; [alpha]-GSU regulation Abstract: Genes and orthologous intrinsic and extrinsic factors critical for embryonic pituitary gonadotrope and thyrotrope cell differentiation have been identified mainly in rodents, but data on the human are very limited. In human fetal pituitaries examined between 14 and 19 weeks of gestation using immunofluorescent confocal microscopy, we found that most fetal gonadotropes expressed [alpha]-GSU, LH[beta], and FSH[beta] gonadotropin subunits while almost no cells expressed [alpha]-GSU and LH[beta] alone. Gonadotropes expressing [alpha]-GSU and FSH[beta] only were detected in both male and female pituitaries, increasing in proportion to total gonadotropes in both males and females from 14 (approximately 4.5%) to 19 weeks (approximately 16.5%) with a peak in males of 45.5% compared with females of 16.5% at 17 weeks of gestation. When FSH[beta] or LH[beta] genes were expressed, gonadotropes were non-dividing. This profile of human fetal gonadotrope development differs from the current mouse model. Furthermore, while expression of [alpha]-GSU appears to be the lead protein in gonadotropes, in thyrotropes which ultimately express [alpha]-GSU with TSH[beta], we observed that most if not all thyrotropes were TSH[beta]-positive but [alpha]-GSU-negative until around 19 weeks in human, and e15 in mouse, fetal pituitaries. Furthermore, the TSH[beta]-only thyrotropes were dividing, and TSH[beta] rather than [alpha]-GSU was the lead protein in thyrotrope development. Thus, while biologically active dimeric FSH and LH can be produced by the human fetal pituitary by 14 weeks, dimeric biologically active TSH will only be produced from around 17 weeks of gestation. The mechanism(s) responsible for the different molecular regulation of [alpha]-GSU gene expression in gonadotropes and thyrotropes in the developing human fetal pituitary now requires investigation. Author Affiliation: Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK Article History: Received 7 December 2005; Revised 11 April 2006; Accepted 5 May 2006

Published
2006

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