Ovarian steroid metabolism during post-natal development in the normal mouse and in the adult hypogonadal (hpg) mouse

Mannan, MA; O’Shaughnessy, Peter J.

doi:10.1530/jrf.0.0820727

Cited by 36 publications

(35 citation statements)

References 23 publications

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“…In this case, THP is formed directly from progesterone, which is produced at high levels from the corpus luteum following ovulation. This pattern of steroid formation is distinct from the rodent (Mannan & O'Shaughnessy, 1988), where the granulosa cells of the ovary form progesterone at high levels prior to ovulation, and following peak levels of estradiol. The rodent has a 4-or 5-day cycle with highest steroid levels on the day of proestrus when circulating levels of progesterone and THP are elevated for 10-12 h in the late PM (Corpechot et al, 1997).…”

Section: Menstrual Cyclementioning

confidence: 81%

“…Steroids, such as 17β-estradiol and THP, remain relatively low in the early phases of puberty but increase throughout development, with peak levels of THP noted during stages IVand V (Fadalti et al, 1999) prior to the onset of fluctuations induced by the menstrual cycle (see below). High circulating and CNS levels of THP have been noted in the mouse and rat immediately before puberty onset (Mannan & O'Shaughnessy, 1988;Palumbo et al, 1995), followed by a decline (Palumbo et al, 1995;Shen et al, 2007).…”

Section: Pubertymentioning

confidence: 99%

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Neurosteroid regulation of GABAA receptors: Focus on the α4 and δ subunits

Smith

Shen

Gong

et al. 2007

Pharmacology & Therapeutics

215

197

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Neurosteroids, such as the progesterone metabolite 3α-OH-5α[β]-pregnan-20-one (THP or [allo] pregnanolone), function as potent positive modulators of the GABA A receptor (GABAR) when acutely administered. However, fluctuations in the circulating levels of this steroid at puberty, across endogenous ovarian cycles, during pregnancy or following chronic stress produce periods of prolonged exposure and withdrawal, where changes in GABAR subunit composition may occur as compensatory responses to sustained levels of inhibition. A number of laboratories have demonstrated that both chronic administration of THP as well as its withdrawal transiently increase expression of the α4 subunit of the GABAR in several areas of the central nervous system (CNS) as well as in in vitro neuronal systems. Receptors containing this subunit are insensitive to benzodiazepine (BDZ) modulation and display faster deactivation kinetics, which studies suggest underlie hyperexcitability states. Similar increases in α4 expression are triggered by withdrawal from other GABA-modulatory compounds, such as ethanol and BDZ, suggesting a common mechanism. Other studies have reported puberty or estrous cycle-associated increases in δ-GABAR, the most sensitive target of these steroids which underlies a tonic inhibitory current. In the studies reported here, the effect of steroids on inhibition, which influence anxiety state and seizure susceptibility, depend not only on the subunit composition of the receptor but also on the direction of Cl -current generated by these target receptors. The effect of neurosteroids on GABAR function thus results in behavioral outcomes relevant for pubertal mood swings, premenstrual dysphoric disorder and catamenial epilepsy, which are due to fluctuations in endogenous steroids.

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Section: Menstrual Cyclementioning

confidence: 81%

Section: Pubertymentioning

confidence: 99%

Neurosteroid regulation of GABAA receptors: Focus on the α4 and δ subunits

Smith

Shen

Gong

et al. 2007

Pharmacology & Therapeutics

215

197

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“…This cell adhesion molecule is present in the surface (or germinal) epithelium of the ovary [19]. Although the levels of endogenous steroids are low in immature mice [20], steroid receptors have been shown to be present in the ovaries of these animals [21]. The growth and differentiation of the surface epithelium is known to be dependent on steroids [22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Estradiol regulates E-cadherin mRNA levels in the surface epithelium of the mouse ovary

1994

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E-cadherin is a calcium-dependent cell adhesion molecule which is present in the surface epithelium of the mouse ovary. This cell adhesion molecule has been implicated as a suppressor of tumorigenesis. The regulators of E-cadherin mRNA levels in the ovary have not been identified. We have examined the ability of steroids to influence ovarian E-cadherin mRNA levels in vivo. Immature mice were injected with either progesterone, testosterone, dihydrotestosterone, 17-beta estradiol or 17-alpha estradiol. Only 17-beta estradiol caused a rapid and significant increase in the ovarian E-cadherin mRNA levels. We speculate that this steroid is a key regulator of E-cadherin-mediated epithelial cell interactions in vivo. We also discuss the possibility that the carcinogenic effects of estrogens on the ovary may be related to their ability to regulate E-cadherin levels in this tissue.

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“…Progesterone and androstenedione were not separated in this system and they were eluted from the first TLC plate and separated by subsequent TLC in chloroform/ether (7/1). The identity of products was confirmed by reverse-phase HPLC using a C18 4 mm column as described previously (Mannan & O'Shaughnessy 1988).…”

mentioning

confidence: 99%

Expression of Cyp21a1 and Cyp11b1 in the fetal mouse testis

Monteiro²,

Johnston³

et al. 2007

Reproduction

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Fetal Leydig cells and fetal adrenocortical cells may share a common progenitor cell. Both cell types show several similarities, particularly in relation to their primary steroidogenic function. Differences in steroid secretion are largely due to the expression of 21-hydroxylase (CYP21A1) and 11b-hydroxylase (CYP11B1) activity in the adrenal. To determine whether expression of these enzymes defines a clear difference between adrenocortical and Leydig cells, or is further evidence of a link between the cell types, we have measured Cyp21a1 and Cyp11b1 expression and related enzyme activity in the fetal testis. Expression of both Cyp21a1 and Cyp11b1 was clearly detectable in the fetal testis by RT-PCR and Southern blotting. Real-time PCR studies showed that Cyp11b1 was expressed only in the fetal/neonatal testis with no expression in the pubertal or post-pubertal animal. Cyp21a1 was also predominantly expressed in the fetal testis although some lower expression was also seen in the adult. Expression of Cyp21a1 and Cyp11b1 in neonatal testicular cells was unaffected by incubation in vitro with human chorionic gonadotrophin or ACTH. Using immunohistochemistry, CYP21A1 was localised to a subset of interstitial steroidogenic cells in the fetal testis although CYP11B1 was not detectable. Incubation studies showed that 21-hydroxylase activity was present in the tissue although 11b-hydroxylase activity could not be detected. Results indicate that a subpopulation of steroidogenic cells in the fetal testis express Cyp21a1 and show 21-hydroxylase activity. This may provide further evidence of a link between fetal Leydig cells and adrenocortical cells but does not discount the possibility that these steroidogenic cells represent 'ectopic' adrenal cells. Reproduction (2007) 134 585-591

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Ovarian steroid metabolism during post-natal development in the normal mouse and in the adult hypogonadal (hpg) mouse

Cited by 36 publications

References 23 publications

Neurosteroid regulation of GABAA receptors: Focus on the α4 and δ subunits

Neurosteroid regulation of GABAA receptors: Focus on the α4 and δ subunits

Estradiol regulates E-cadherin mRNA levels in the surface epithelium of the mouse ovary

Expression of Cyp21a1 and Cyp11b1 in the fetal mouse testis

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