Testosterone, dihydrotestosterone and estradiol-17β levels in maternal and fetal plasma and in fetal testes in the rat

Habert, René; Picon, R.

doi:10.1016/0022-4731(84)90383-2

Cited by 136 publications

(84 citation statements)

References 27 publications

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“…Testosterone was extracted from the serum and assayed by RIA as previously described. 46 Reverse-transcription and real-time PCR. Reverse transcription was carried out with 250 ng of total RNA recovered from ovaries of mice aged 2 months, 400 ng oligo-dT primers (Qiagen, Courtaboeuf, France) and Superscript II reverse transcriptase (Invitrogen, Cergy Pontoise, France).…”

Section: Discussionmentioning

confidence: 99%

Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells

Vandormael-Pournin¹,

Guigon²,

Coudouel³

et al. 2014

Cell Death Differ

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Aberrant loss of oocytes following cancer treatments or genetic mutations leads to premature ovarian insufficiency (POI) associated with endocrine-related disorders in 1% of women. Therefore, understanding the mechanisms governing oocyte death is crucial for the preservation of female fertility. Here, we report the striking reproductive features of a novel mouse model of POI obtained through oocyte-specific inactivation (ocKO) of Omcg1/Zfp830 encoding a nuclear zinc finger protein involved in premRNA processing. Genetic ablation of OMCG1 in early growing oocytes leads to reduced transcription, accumulation of DNA double-strand breaks and subsequent c-Abl/TAp63-dependent oocyte death, thus uncovering the key role of OMCG1 for oocyte genomic integrity. All adult Omcg1 ocKO females displayed complete elimination of early growing oocytes and sterility. Unexpectedly, mutant females exhibited a normal onset of puberty and sexual receptivity. Detailed studies of Omcg1 ocKO ovaries revealed that the ovarian somatic compartment underwent a dramatic structural and functional remodeling. This allowed the cooperation between oocyte-depleted follicles and interstitial tissue to produce estradiol. Moreover, despite early folliculogenesis arrest, mutant mice exhibited sexual cyclicity as shown by cyclical changes in estrogen secretion, vaginal epithelium cytology and genital tract weight. Collectively, our findings demonstrate the key role of Omcg1 for oocyte survival and highlight the contribution of p63 pathway in damaged oocyte elimination in adulthood. Moreover, our findings challenge the prevailing view that sexual cyclicity is tightly dependent upon the pace of folliculogenesis and luteal differentiation.

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Section: Discussionmentioning

confidence: 99%

Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells

Vandormael-Pournin¹,

Guigon²,

Coudouel³

et al. 2014

Cell Death Differ

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“…Active production of testosterone starts by 15.5 dpc, with production increasing markedly thereafter (Habert and Picon, 1984). The steroidogenic capacity per fetal Leydig cell is higher than that in ALCs, which are subject to negative control by hormonal and paracrine factors (Huhtaniemi and Pelliniemi, 1992).…”

Section: Regulation Of Steroidogenesis In Fetal Leydig Cellsmentioning

confidence: 98%

Key factors in the regulation of fetal and postnatal leydig cell development

Wan

Lee

2007

Journal Cellular Physiology

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The primary function of testicular Leydig cells is the production of androgens to promote sexual differentiation in the fetus, secondary sexual maturation at puberty, and spermatogenesis in the adult. The fetal and postnatal (adult) populations of Leydig cells differ morphologically and have distinct profiles of gene expression. As postnatal Leydig cells differentiate, they transition through three discrete maturational stages characterized by decreasing proliferative rate and increasing testosterone biosynthetic capacity. In this review, we discuss the development of both fetal and postnatal Leydig cells and review the regulation of this process by some of the key hormones and growth factors.

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“…In rats, FLCs start to differentiate and produce testosterone at gestational age of 14 days before they undergo functional regression from fetal day 18.5 onward (Habert and Picon, 1984;Kuopio et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

Weisser¹,

Landreh²,

Söder³

et al. 2011

Molecular and Cellular Endocrinology

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Please cite this article as: Weisser, J., Landreh, L., Söder, O., Svechnikov, K., Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells, Molecular and Cellular Endocrinology (2008), doi:10.1016/j.mce.2011 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Our data indicate that cAMP-activated signaling pathway(s) play an important role in the regulation of PFLCs differentiation and function.

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Testosterone, dihydrotestosterone and estradiol-17β levels in maternal and fetal plasma and in fetal testes in the rat

Cited by 136 publications

References 27 publications

Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells

Oocyte-specific inactivation of Omcg1 leads to DNA damage and c-Abl/TAp63-dependent oocyte death associated with dramatic remodeling of ovarian somatic cells

Key factors in the regulation of fetal and postnatal leydig cell development

Steroidogenesis and steroidogenic gene expression in postnatal fetal rat Leydig cells

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