Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.1.1.3 (HSD)
3,464 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were carried out to investigate the abundance of mRNA for luteotrophic receptors and steroidogenic elements in the ovaries and corpora lutea of mink during the embryonic diapause, peri-implantation and postimplantation pregnancy. The second aim was to determine whether the mink placenta synthesized progesterone. Homologous cDNA probes for the mink LH and prolactin receptors were generated by the polymerase chain reaction. Heterologous cDNA probes for steroidogenic acute regulatory protein (StAR), cytochrome P450 side chain cleavage (P450scc) and 3 beta-hydroxysteroid dehydrogenase-delta 4-delta 5 isomerase (3 beta HSD) were also used. The abundance of mRNA encoding the prolactin receptor was low during the period of embryonic diapause and increased concurrent with circulating progesterone. The abundance of LH receptor message reached peak values during the peri-implantation period followed by maintenance of a steady-state after implantation. The abundance of StAR and P450scc messages appeared not to vary during gestation, while that for 3 beta HSD was correlated with changes in circulating progesterone. There was no evidence of 3 beta HSD activity or transcripts in the placenta. These results indicate that prolactin and LH are necessary for activation of the corpus luteum during the period of embryonic diapause, and for its maintenance during postimplantation gestation. The mink placenta does not synthesize progesterone.
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PMID:Luteal and placental characteristics of carnivore gestation: expression of genes for luteotrophic receptors and steroidogenic enzymes. 940 81

Ovarian follicular development in cattle is characterized by waves of growth during the prepubertal and postpartum periods and during estrous cycles. Each wave of follicular growth is characterized by recruitment of a cohort of follicles 4 to 5 mm in diameter. From the cohort, one follicle is selected for continued growth and becomes dominant. If luteolysis occurs during the growth phase of dominant follicles, final maturation and ovulation occurs. If luteolysis does not occur during the growing and maintenance phase of follicles, the fate is atresia. Changes in mRNA expression for the gonadotropin receptors (FSHr and LHr), key steroidogenic enzymes (cytochrome P450 side chain cleavage [P450scc], cytochrome P450 17alpha-hydroxylase-[P450c17], cytochrome P450 aromatase [P450arom], and 3beta-hydroxysteroid dehydrogenase [3beta-HSD]), and growth factors (IGF-I and -II) and their binding proteins (IGFBP) have been associated with different stages of follicular growth and atresia. In general, expression of mRNA for the gonadotropin receptors, steroidogenic enzymes, and steroidogenic acute regulatory protein (StAR) increase with progressive follicular development and is highest when dominant follicles approach maximum size. Expression of mRNA declines rapidly and becomes low or undetectable in atretic follicles. The IGF-I (granulosal cells) and IGF-II (thecal cells) are increased, whereas IGFBP-2 (granulosal cells) is reduced, in dominant follicles. Recruitment of a cohort of follicles is associated with initiation of expression of mRNA for P450scc and P450arom in granulosal cells. Selection of dominant follicles is associated with expression of mRNA for LHr and 3beta-HSD in granulosal cells. Thus, changes in gene expression likely are important to recruitment, selection, dominance, and atresia in ovarian follicles.
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PMID:Expression of steroidogenic enzyme and gonadotropin receptor genes in bovine follicles during ovarian follicular waves: a review. 969 Jun 47

DAX-1 is an unusual member of the nuclear hormone receptor superfamily whose expression is mainly, but not uniquely, restricted to steroidogenic tissues. We have recently shown that DAX-1 can block the first and rate-limiting step in steroid biosynthesis by repressing StAR (steroidogenic acute regulatory protein) expression. Here we show that DAX-1 blocks steroid production at multiple levels in the Y-1 mouse adrenocortical tumor cell line. Expression of DAX-1 in Y-1 cells significantly impairs both basal and cAMP-stimulated steroid production, without affecting the functionality of the cAMP-responsive PKA pathway. Experiments using an hydroxylated cholesterol derivative show that biochemical steps in steroidogenesis subsequent to cholesterol delivery to mitochondria are also impaired in Y-1 cells expressing DAX-1. This is explained by the repression of P450scc and 3beta-HSD expression, in addition to StAR. DAX-1 expression in Y-1 cells results in the inhibition of the activity of the StAR, P450scc and 3beta-HSD promoters. An inappropriate steroidogenic block in the male fetus might have an important role in the pathogenesis of sex reversal syndromes caused by a duplication of the genomic region of the X chromosome containing the DAX-1 gene.
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PMID:DAX-1 blocks steroid production at multiple levels. 975 5

Gonadal development and differentiation is dependent in part on GH, as GH deficiency has been implicated as a cause of lowered fertility and spermatogenic cessation in humans and some biological models. In this study, we demonstrate that GH receptor messenger RNA (mRNA) is preferentially expressed in progenitor Leydig cells (PLCs) isolated and purified from 21-day-old rats. GH induces significant increases in the levels of steroidogenic acute regulatory protein (StAR), 3beta-hydroxysteroid dehydrogenase (3beta-HSD) expression, and androgen production in PLCs. Additionally, the cytokine interferon-gamma (IFNgamma) markedly inhibits GH-stimulated StAR mRNA and protein levels. When cells are cultured with both GH and IFNgamma, IFNgamma decreases the stimulating effect of GH on androgen production. Treatment of PLCs with cycloheximide does not prevent the GH-induced StAR mRNA, indicating that GH induction of StAR transcripts does not require de novo protein synthesis. In contrast, the induction of 3beta-HSD mRNA by GH is altered by cycloheximide treatment. H7, a serine/threonine kinase inhibitor, completely abrogates the increases in StAR mRNA by GH, whereas the tyrosine kinase inhibitor genistein does not. Moreover, GH further enhances StAR and 3beta-HSD mRNA expression in isolated adult rat Leydig cells despite their increased basal expression subsequent to maturational acquisition of these steroidogenic components. These data provide the first demonstration of the direct effects of GH on testicular steroidogenesis during progenitor Leydig cell differentiation.
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PMID:Growth hormone regulates steroidogenic acute regulatory protein expression and steroidogenesis in Leydig cell progenitors. 1009 3

Steroidogenic factor-1 (SF-1) is a transcription factor involved in regulating basal and/or cAMP-induced increases in expression of several components of the steroidogenic pathway, including cytochrome P450 side-chain cleavage (P450scc), steroidogenic acute regulatory protein (StAR), and 3beta-hydroxysteroid dehydrogenase/delta5, delta4 isomerase (3beta-HSD). In experiment 1, on days 3, 6, 9, 12, and 15 of the estrous cycle, steady-state concentrations (fmol/microg poly A+ RNA) of SF-1 mRNA in luteal tissue were 0.09 +/- 0.01, 0.17 +/- 0.01, 0.24 +/- 0.03, 0.30 +/- 0.09, and 0.20 +/- 0.05, respectively (estrus = day 0; n = 4/d). Concentrations of SF-1 mRNA increased (p < 0.05) between days 3 and 12, but were not different among the other days of the estrous cycle. Luteal concentrations of SF-1 mRNA and concentrations of progesterone in sera were highly correlated (p < 0.01; r = 0.72). In experiment 2, ewes on days 11 or 12 of the estrous cycle were injected with 25 mg prostaglandin F2alpha (PGF2alpha) into the jugular vein followed by an injection of 10 mg PGF2alpha i.m. 2 h later. Corpora lutea were collected 4, 12, and 24 h after the first injection of PGF2alpha (n = 4-5 ewes/time). Control luteal tissue was collected from ewes on days 11-13 of the estrous cycle, which had not been injected (n = 4) or had been injected with saline 24 h previously (n = 4). Steady-state concentrations of SF-1 mRNA had decreased (p < 0.05) to 48% of control values by 4 h after injection, and remained low at 12 and 24 h. In experiment 3, ewes on days 9-12 of the estrous cycle were administered PGF2alpha (1 micromol), phorbol 12-myristate 13-acetate (PMA; 2 micromol), luteinizing hormone (LH; 20 microg), forskolin (50 microg), or vehicle (1 mL saline) directly into the ovarian artery. Corpora lutea were collected 0 (noninfused) 4, 12, or 24 h later (n = 3-4 animals/treatment/time) for quantification of SF-1 mRNA. Steady-state concentrations of mRNA encoding SF-1 were not affected by infusion of PGF2alpha or PMA, although concentrations of mRNA encoding StAR and 3beta-HSD were decreased (p < 0.05) by these treatments. Concentrations of mRNA encoding SF-1 were increased (p < 0.05) to 157 and 149% of control values by LH and forskolin, respectively, 12 h following infusion and returned to control values by 24 h following either treatment. In contrast, infusion of LH or forskolin did not change concentrations of mRNA encoding StAR, P450scc, or 3beta-HSD. In summary, during the estrous cycle, the pattern of expression of SF-1 mRNA was similar to the pattern of concentrations of progesterone in serum and expression of mRNA encoding P450scc, but differed from that previously shown for 3beta-HSD and StAR mRNA. The effects of administration of PGF2alpha on concentrations of SF-1 mRNA appeared to be dose-dependent. However, acute effects of PGF2alpha on mRNA encoding 3beta-HSD and StAR were observed when concentrations of mRNA encoding SF-1 were not influenced. In addition, although LH or forskolin increased luteal SF-1 mRNA 12 h following infusion, no increases in mRNA encoding StAR, P450scc, or 3beta-HSD were observed. Thus, during the midluteal phase of the estrous cycle, neither luteotropic nor luteolytic hormones appear to coordinately regulate mRNA encoding SF-1 and mRNA encoding StAR, P450scc, or 3beta-HSD.
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PMID:Luteal expression of steroidogenic factor-1 mRNA during the estrous cycle and in response to luteotropic and luteolytic stimuli in ewes. 1022 87

In a human conception cycle, the expected decline in progesterone production by the corpus luteum during the late luteal phase is prevented by human chorionic gonadotrophin (HCG) secreted by the implanting blastocyst. This study investigated the expression of components of the synthetic pathway for progesterone in human corpora lutea in the presence and absence of HCG in vivo. Corpora lutea were obtained from: (i) normally cycling women at the time of hysterectomy and classified on the basis of the urinary luteinizing hormone (LH) surge as early (n = 3), mid- (n = 3), or late luteal (n = 3); or (ii) women who had received daily doubling doses of HCG (n = 3) to 'rescue' the corpus luteum. Expression patterns of steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side-chain cleavage (P450scc) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) were investigated by Northern blotting, in-situ hybridization and immunohistochemistry. Luteal 'rescue' with HCG was associated with the continued expression of these components. In the late luteal phase, in the absence of HCG, expression remained but was more variable. The expression of 3beta-HSD mRNA was significantly reduced during the luteal phase (P<0.01). In conclusion, during luteal 'rescue', HCG acts to maintain the steroidogenic pathway. In the absence of HCG, the decline in progesterone production begins in the presence of the main components of the steroidogenic pathway. While unlikely to initiate this decline, the altered expression levels of these components, particularly that of 3beta-HSD, may contribute to the continued reduction in progesterone production.
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PMID:Steroidogenic enzyme expression in human corpora lutea in the presence and absence of exogenous human chorionic gonadotrophin (HCG). 1032 99

Although progesterone plays an essential role in ovulation and the luteiniziation of the primate follicle, the expression of cellular components required for progesterone synthesis and their control is not well defined. This study was designed to determine the time course and gonadotrophin versus steroid regulation of the transcription of genes involved in progesterone synthesis in peri-ovulatory follicles. Granulosa cells or whole ovaries were obtained from macaques undergoing controlled ovarian stimulation either before (0 h) or up to 36 h following the administration of an ovulatory human chorionic gonadotrophin (HCG) bolus with or without a 3beta-hydroxysteroid dehydrogenase (3beta-HSD) inhibitor, with or without a non-metabolizable progestin. Granulosa cell concentrations of low density lipoprotein receptor (LDL-R) and steroidogenic acute regulatory protein (StAR) mRNA increased transiently 12 h following HCG administration (P < 0.05) at which time steroid depletion tended to reduce StAR mRNA (P = 0.06). At 36 h post-HCG progesterone suppressed the LDL-R mRNA levels (P < 0.05). P450 side-chain cleavage (P450scc) mRNA decreased in a time-dependent fashion up to 24 h, whereas 3beta-HSD mRNA increased within 12 h of HCG administration (P < 0.05) in a steroid-independent manner. Whole ovarian 17alpha-hydroxylase (P450c17) and granulosa cell P450 aromatase (P450arom) mRNA declined in a time-dependent fashion; by 36 h after HCG administration, steroid depletion increased P450arom mRNA, although progestin replacement did not return aromatase to control values (P < 0.05). These data demonstrate diverse patterns of steroidogenic enzyme expression that generally reflect the conversion of the macaque peri-ovulatory follicle from an oestrogen to progesterone producing gland. Although mRNAs associated with progesterone synthesis and metabolism are primarily regulated by gonadotrophins, cholesterol uptake and utilization may be modulated locally by steroids in luteinizing granulosa cells.
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PMID:Hormonal regulation of steroidogenic enzyme expression in granulosa cells during the peri-ovulatory interval in monkeys. 1061 Dec 55

Gap junctions are intercellular protein channels which provide a pathway for the exchange of ions and small molecules. This exchange of materials allows metabolic coupling of cells. Gap junction channels are made up of connexins, integral membrane proteins encoded by a multigene family. Rat testes contain mRNAs for at least five different connexins: Cx26, Cx32, Cx33, Cx37 and Cx43. Immunocytochemical studies have shown that Cx43 assembles gap junctions between Leydig cells. The present study investigated the expression and regulation of the Cx43 gene in rat Leydig cells. Purified Leydig cells were obtained from 40- to 80-day-old Sprague-Dawley rats using a combination of arterial perfusion, collagenase digestion, centrifugal elutriation and Percoll gradient centrifugation. Leydig cells from 20- and 30-day-old rats were isolated without arterial perfusion or centrifugal elutriation. Cx43 mRNA was present in 20-day-old rat Leydig cells, reached a plateau at day 40, and remained at high levels in 65- and 80-day-old rat Leydig cells. To evaluate the regulation of Cx43 gene expression, Leydig cells were cultured overnight and then treated with human chorionic gonadotropin (hCG) for variable periods of time. Addition of hCG (10 ng/ml) increased cytochrome P450 side-chain cleavage and steroidogenic acute regulatory protein mRNA levels and testosterone formation. However, Cx43 mRNA levels were inhibited by hCG in a time- and dose-dependent manner. Cx43 mRNA levels decreased 27% as early as 2 h after the addition of hCG and decreased 60% by 24 h. Treatment of Leydig cells with 8-bromo-cAMP (0.1 mM) for 6 and 24 h also reduced Cx43 mRNA levels by 36 and 56% respectively. Primary cultured Leydig cells stained strongly positive with anti-Cx43 monoclonal antibody. Treatment with hCG for 24 h reduced Cx43 signals and caused Cx43 to redistribute to the periphery of the cells. To evaluate the regulation of Cx43 in vivo, rats were treated with hCG (300 ng i.p.) and testes were removed 24 h later. Frozen section of testes revealed that these interstitial cells stained positive for 3beta-hydroxysteroid dehydrogenase (3beta-HSD) by histochemical staining and were positive for Cx43 by immunofluorescence staining. The adjacent seminiferous tubules stained only weakly positive for Cx43. Twenty-four hours after hCG treatment, 3beta-HSD activity increased while Cx43 immunostaining of Leydig cells was reduced. In conclusion, gap junction channels of Leydig cells are regulated by hCG both in vivo and in vitro. hCG increased Leydig cell steroidogenesis and steroidogenic enzyme mRNA levels but caused a redistribution of Cx43.
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PMID:Expression and regulation of connexin43 in rat Leydig cells. 1092 34

Steroid hormones secreted by fetal adrenocortical cells are considered to be a requirement for a fetus to maintain intrauterine life, but, to date, the regulation of steroid hormone secretion has not been studied in detail in the human fetal adrenal gland. In this study, we examined the immunolocalization of steroidogenic enzymes and their local regulation, including adrenal 4-binding protein (Ad4BP or NR5A1), steroidogenic acute regulatory protein (StAR), P450 cholesterol side-chain cleavage (P450scc or CYP11A1), P450 17alpha-hydroxylase/17,20-lyase (P450c17 or CYP17), 3beta-hydroxysteroid dehydrogenase/isomerase (3beta-HSD), P450 21 hydroxylase (P450c21 or CYP21), dehydroepiandrosterone sulfotransferase (DHEA-ST), P450 oxidoreductase and cytochrome b5, in the human fetal adrenal gland (n=31) obtained from fetuses ranging in ages from 14 to 40 weeks of gestation. Ad4BP immunoreactivity was detected in all adrenocortical zones throughout gestation, suggesting that this nuclear protein is likely to be essential in the development of the human adrenal. Immunoreactivity for StAR, P450scc, P450c21, P450 oxidoreductase and cytochrome b5 was detected only in fetal and transitional zone between 14 and 22 weeks of gestation, but was detected in all three zones after 23 gestational weeks. 3beta-HSD immunoreactivity was not detected in any of the three cortical zones prior to 22 weeks of gestation, but became discernible in the transitional zone and definitive zone after 23 weeks. Immunoreactivity for P450c17 and DHEA-ST was detected in the transitional and fetal zones throughout gestation, but not in the definitive zone. These results suggest that the human adrenal cortex may produce dehydroepiandrosterone (DHEA) in the transitional and fetal zones throughout gestation, and cortisol in the transitional zone after the 23rd week of gestation.
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PMID:Temporal and spatial distribution of corticosteroidogenic enzymes immunoreactivity in developing human adrenal. 1130 77

The aim of this study was to determine 1) the time of onset and cellular localization of gene expression for steroidogenic factor-1 (SF-1), steroidogenic acute regulatory protein, 3beta-hydroxysteroid dehydrogenase/Delta(5),Delta(4) isomerase (3beta-HSD), and the cytochrome P450 enzymes for cholesterol side-chain cleavage (P450(scc)), 17alpha-hydroxylase (P450(17alphaOH)), and aromatase (P450(arom)) during gonadal development; and 2) the amount of progesterone, androstenedione, testosterone, and 17beta-estradiol present in the fetal sheep gonad. Fetuses were collected on Days 24, 26, 28, 30, 32, 35, 40, 55, and 75 of gestation, and gene expression was determined by in situ hybridization. The steroid content of gonads collected on Days 30, 35, 55, and 75 of gestation was determined by RIA. Developing gonads collected from both male and female fetuses were steroidogenically active around the time of morphological sexual differentiation. In the female, the steroidogenic cells were initially located at the boundary of the cortex and medulla but become increasingly restricted to the mesonephric-derived cell streams. In the male, once tubules were identifiable, steroidogenesis was restricted to the interstitial regions. Interestingly, expression of both SF-1 and 3beta-HSD was observed prior to morphological sexual differentiation. In addition, expression of both of these genes was more widespread than the other genes in both males and females.
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PMID:Ontogeny of steroidogenesis in the fetal sheep gonad. 1142 Feb 43


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