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)

P450scc and 3beta-HSD cDNA were isolated from a zebrafish lambda gt10 cDNA library using trout SCC and 3beta-HSD cDNA as the probes. The zebrafish SCC cDNA encodes a protein of 509 amino acids, which shares a 78% similarities with the trout SCC and 58% with the human SCC. As for 3beta-HSD, two forms of cDNA were isolated, termed HSD 5 and HSD 17, which may have resulted from alternative splicing. HSD 5 and HSD 17 encode proteins of 374 and 341 amino acids respectively. Both share 77% amino acid similarities with trout 3beta-HSD and 53% similarities with the mouse 3beta-HSD. Zebrafish has been increasingly used as a genetic model system to study organ development and to investigate human diseases. The cloning and the characterization of zebrafish P450scc and 3beta-HSD should facilitate study of steroidogenesis and human disease associated with steroid imbalance.
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PMID:Cloning of zebrafish cDNA for 3beta-hydroxysteroid dehydrogenase and P450scc. 988 98

Recently, we have demonstrated, using biochemical and immunochemical methods, that the quail brain possesses the cholesterol side-chain cleavage enzyme (cytochrome P450scc) and produces pregnenolone and its sulfate ester. To clarify progesterone biosynthesis in the avian brain, therefore, we examined the expression of messenger RNA (mRNA) encoding for the enzyme 3beta-hydroxysteroid dehydrogenase/Delta5-Delta4-isomerase (3beta-HSD) and its enzymatic activity using the quail. RT-PCR analysis together with Southern hybridization indicated the expression of 3beta-HSD mRNA in the brain of sexually mature birds but with no clear-cut sex difference. Employing biochemical techniques combined with HPLC analysis, the conversion of pregnenolone to progesterone was found in brain slices of mature males. Progesterone biosynthesis was increased in a time dependent manner and completely abolished by trilostane, a specific inhibitor of 3beta-HSD. The enzymatic activity of 3beta-HSD was greatest in the cerebrum and lowest in the mesencephalon. A specific RIA indicated that progesterone concentrations in the different brain regions closely followed the level of 3beta-HSD activity. High levels of progesterone concentration were observed in the diencephalon and cerebrum with lowest values in the mesencephalon. Progesterone levels in the brain regions were significantly higher than those in the plasma. These results suggest that the avian brain possesses not only cytochrome P450scc but also 3beta-HSD and produces progesterone. It is also indicated that progesterone biosynthesis in the avian brain may be region-dependent.
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PMID:Expression and activity of 3beta-hydroxysteroid dehydrogenase/Delta5-Delta4-isomerase in different regions of the avian brain. 1008 43

We investigated the regulation of steroidogenesis in a cell line of porcine granulosa origin, JC-410. Cells responded to the protein kinase-A activators, cholera toxin and forskolin, with increased accumulation of intracellular cAMP. Histochemically, cells were shown to contain 3beta-HSD, the enzyme which converts pregnenolone to progesterone. The JC-410 cells produced progesterone and responded to the protein kinase-A activators with an increase in progesterone synthesis. Progesterone levels were also increased by 25-hydroxycholesterol, pregnenolone, estradiol and androstenedione. Follicle-stimulating hormone and luteinizing hormone had no effect on cAMP or progesterone accumulation. Androstenedione was required for the synthesis of estradiol by JC-410 cells. Steady-state levels of mRNA for the steroidogenic enzymes 3beta-HSD and P450scc were increased by treatment with cholera toxin, whereas P450arom was not changed. These cells express the steroidogenic enzymes genes in a similar fashion to primary cultures of porcine granulosa cells. The JC-410 cells may represent a valuable model to study second messenger regulation and the molecular mechanisms involved in steroidogenesis in granulosa cells.
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PMID:Regulation of steroidogenesis in jc-410, a stable cell line of porcine granulosa origin. 1022 74

The objective of this investigation was to determine the effect of steroid hormones on the synthesis of progesterone in a stable porcine granulosa cell line, JC-410. We also examined the effect of steroid hormones on expression of the genes encoding the steroidogenic enzymes, cytochrome P450-cholesterol side chain cleavage (P450scc) and 3beta-hydroxy-5-ene steroid dehydrogenase (3beta-HSD). We observed that 48 h exposure of the JC-410 cells to estradiol-17beta (estradiol), androstenedione, 5alpha-dihydrotestosterone, levonorgestrel, and 5-cholesten-3beta, 25-diol (25-hydroxycholesterol) resulted in stimulation of progesterone synthesis. 25-Hydroxycholesterol augmented progesterone synthesis stimulated by estradiol, 5alpha-dihydrotestosterone, levonorgestrel and 8-bromoadenosine 3':5'-cyclic monophosphate (8-Br-cAMP). This increase in progesterone synthesis was additive with estradiol, 5alpha-dihydrotestosterone and levonorgestrel, and synergistic with 8-Br-cAMP. Cholera toxin, progesterone, levonorgestrel and androstenedione increased P450scc mRNA levels, whereas estradiol had no effect. Cholera toxin, progesterone and levonorgestrel increased 3beta-HSD mRNA levels, but estradiol and androstenedione had no effect. The results were interpreted to mean that estrogens, androgens and progestins regulate progesterone synthesis in the JC-410 cells. The effect of androgens appears to be mediated by stimulation of P450scc gene expression while progestins stimulate both P450scc and 3beta-HSD gene expression. Our results support the concept that progesterone is an autocrine regulator of its own synthesis in granulosa cells.
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PMID:Steroid regulation of progesterone synthesis in a stable porcine granulosa cell line: a role for progestins. 1041 31

Ovarian follicular growth and development is an integrated process encompassing both extraovarian signals, such as gonadotrophins and metabolic hormones, and intraovarian factors. Follicular development has been classified into gonadotrophin-independent and -dependent phases. In the latter, FSH provides the primary drive for follicular recruitment and LH is required for continued development of follicles to the preovulatory stage. A transient increase in circulating FSH precedes the recruitment of a group of follicles, and these recruited follicles are characterized by expression of mRNAs encoding P450scc and P450arom in granulosal cells. As follicles mature, there is a transfer of dependency from FSH to LH, which may be part of the mechanism(s) involved in selection of follicles for continued growth. Indeed, changes in the pattern of expression of mRNA for gonadotrophin receptors and steroid enzymes within follicular cells appear to be closely linked to changes in peripheral concentrations of gonadotrophins. The mechanism of selection of dominant follicles still requires clarification, but seems to be linked to the timing of mRNA expression encoding LHr and 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) in granulosal cells. Additional intraovarian systems, including the ovarian IGF and activin/inhibin systems, also exert a role. For example, it appears that the development of follicular dominance in cows is associated with the FSH-dependent inhibition of the expression of mRNA encoding insulin-like growth factor binding protein 2 (IGFBP-2) in granulosal cells. In conclusion, the integration of these endocrine signals and intraovarian factors within follicles determines whether follicles continue to develop and become dominant or are diverted into apoptotic pathways leading to atresia.
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PMID:Molecular mechanisms regulating follicular recruitment and selection. 1069 43

Expression of cytochrome P450 cholesterol side chain cleavage (P450scc) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) mRNAs was examined in chicken embryonic adrenal glands and gonads between days 4 and 12 of incubation. In situ hybridization analysis showed that 3beta-HSD mRNA appeared on day 5 of incubation in the adrenal glands and on day 6 in the gonads, while P450scc mRNA was expressed on day 7 in both the adrenal glands and the gonads. Cells expressing both enzyme mRNAs were distributed in the steroidogenic tissues of the adrenal glands and in the medullary cords of the gonads. From days 9 to 11 of incubation, P450scc mRNA expression was not found in the majority of both the adrenal glands and the gonads, but was detected again in both on day 12, although 3beta-HSD mRNA was constitutively expressed during this period. Changes in the expression pattern of P450scc mRNA are paralleled by changes in the plasma corticosterone level reported previously. Therefore, it is suggested that P450scc is essential to embryogenesis.
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PMID:Expression of cytochrome P450 cholesterol side chain cleavage and 3beta-hydroxysteroid dehydrogenase during embryogenesis in chicken adrenal glands and gonads. 1075 71

To find an explanation for the possible working mechanism of laparoscopic ovarian electrocautery for the treatment of anovulation in polycystic ovarian syndrome (PCOS), we evaluated the distribution of steroidogenic enzymes involved in the synthesis of ovarian androgens in surgical pathology specimens of entire polycystic ovaries. A total of 13 formalin-fixed and paraffin-embedded samples of the ovaries of patients with clinically proven PCOS were immunostained with specific antibodies against cholesterol side-chain-cleavage enzyme (P450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), 17alpha-hydroxylase (P450c17) and adrenal 4-binding protein (Ad4BP), a transcription factor of steroidogenic enzymes. Follicular theca cells of all ovaries demonstrated marked immunoreactivity for Ad4BP, P450scc, 3beta-HSD and P450c17. Granulosa cells of seven ovaries expressed Ad4BP, while granulosa cells of three ovaries also showed P450scc. In the granulosa cells of all ovaries, 3beta-HSD and P450c17 immunoreactivity was not observed. In the stroma, luteinized cells of most ovaries demonstrated Ad4BP, P450scc, 3beta-HSD and P450c17 immunoreactivity, but at a much lower level compared with the follicular theca cells. Non-luteinized stromal cells sporadically demonstrated Ad4BP, P450scc, 3beta-HSD and P450c17 immunoreactivity. The stromal steroidogenic cells were mainly located in the ovarian cortex, except for some hilus steroidogenic cells. These data demonstrate that in polycystic ovaries, androgens are mainly produced in the follicular theca cells and to some extent in luteinized stromal cells. This suggests that the working mechanism of laparoscopic electrocautery of the ovary is primarily explained through the reduction of ovarian hyperandrogenism by coagulation of follicular theca cells and concomitant stroma.
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PMID:Distribution of steroidogenic enzymes involved in androgen synthesis in polycystic ovaries: an immunohistochemical study. 1077 48

Previously, progesterone was found to regulate the initiation and biosynthetic rate of myelin synthesis in Schwann cell/neuronal cocultures. The mRNA for cytochrome P450scc (converts cholesterol to pregnenolone), 3beta-hydroxysteroid dehydrogenase (3beta-HSD, converts pregnenolone to progesterone), and the progesterone receptor were found to be markedly induced during active myelin synthesis. However, the cells in the cocultures responsible for these changes were not identified. In this study, in situ hybridization was used to determine the localization of the enzymes responsible for steroid biosynthesis. The mRNA for cytochrome P450scc and 3beta-HSD were detected only in actively myelinating cocultures and were localized exclusively in the Schwann cells. Using immunocytochemistry, with minimal staining of the Schwann cells, we found the progesterone receptor in the dorsal root ganglia (DRG) neurons. The progesterone receptor in the neurons translocated into the nuclei of these cells when progesterone was added to neuronal cultures or during myelin synthesis in the cocultures. Additionally, a marked induction of the progesterone receptor was found in neuronal cultures after the addition of progesterone. The induction of various genes in the neurons was also investigated using mRNA differential display PCR in an attempt to elucidate the mechanism of steroid action on myelin synthesis. Two novel genes were induced in neuronal cultures by progesterone. These genes, along with the progesterone receptor, were also induced in cocultures during myelin synthesis, and their induction was blocked by RU-486 (a progesterone receptor antagonist). These genes were not induced in Schwann cells cultured alone after the addition of progesterone. These results suggest that progesterone is synthesized in Schwann cells and that it can indirectly regulate myelin formation by activating transcription via the classical steroid receptor in the DRG neurons.
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PMID:Progesterone synthesized by Schwann cells during myelin formation regulates neuronal gene expression. 1088 68

Sex steroid hormones exert important influences on neuroendocrine and behavioural brain function. As neuroactive steroids they are able to modify neuronal excitability. Unbalanced synthesis may thus be implicated in pathophysiological conditions, such as epilepsy, migraine, depression and anxiety. In sex steroid metabolism, 17beta-hydroxisteroid dehydrogenases (17beta-HSDs) play a crucial role in catalyzing the final steps of androgen and estrogen biosynthesis. The hippocampus appears to be a major target area of neurosteroidal action. The expression of 17beta-HSD isozymes has not yet been studied in human hippocampus. Therefore, we investigated the expression of 17beta-HSD 1, 2, 3 and 4 mRNAs in hippocampal tissue specimens obtained at neurosurgery from 42 patients with pharmacoresistant temporal lobe epilepsy. A competitive RT-PCR assay was used to quantify the mRNA transcript level. 17beta-HSD 1 mRNA concentrations were 10000 fold lower in the hippocampus compared to placental tissue, whereas 17beta-HSD 3 mRNA concentrations were 50 fold lower than in testis and 17beta-HSD 4 concentrations were in the same order of magnitude as in liver. 17beta-HSD 2 mRNA was not expressed. 17beta-HSD 1, 3 and 4 mRNA concentrations in the hippocampus showed no significant differences between men and women and there were no significant differences in expression levels of these enzymes between patients with Ammon's horn sclerosis (AHS) and those with histopathologically normal hippocampus associated with extrahippocampal lesions. No significant correlation could be detected between duration of epilepsy, individual seizure frequency and expression levels of 17beta-HSDs. In conclusion, the present study is the first to demonstrate mRNA expression of 17beta-HSD 1, 3 and 4 in the epileptic human hippocampus. Together with data on 5alpha-reductase 1, 3alpha-hydroxisteroid oxidoreductase 2 and cytochrome P450scc, previously shown to be expressed in the human hippocampus also, our data provide further evidence for the existence of sex steroid formation and metabolism in this specific brain area.
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PMID:Expression of mRNAs encoding for 17beta-hydroxisteroid dehydrogenase isozymes 1, 2, 3 and 4 in epileptic human hippocampus. 1092 71

We investigated the roles of estrogens and androgens in the progesterone biosynthesis of bovine luteal cells. The responsiveness of primary luteal cells to the stimulation of tropic agents was observed in a dose-dependent manner. Estrogens and androgens significantly inhibited tropic agent-induced progesterone secretions, but glucocorticoids did not, which indicated the inhibitions were specific. The failure of exogenous 8-Br-cAMP to prevent these inhibitions suggested that took place at the post-cAMP steps. The immunoblot showed that testosterone remarkably decreased the amount of induced P450scc protein after 6-hour treatment, yet 17beta-estradiol did not. The 3beta-HSD activity assays demonstrated that both 17beta-estradiol and testosterone efficiently blocked induced 3beta-HSD activities. Both inhibitory effects of E2 and T on progesterone synthesis were observed one hour after treatment and accompanied with suppressed 3beta-HSD activities. This study presents that estrogens and androgens specifically inhibit bovine luteal function through different mechanisms.
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PMID:Differential inhibition of progesterone synthesis in bovine luteal cells by estrogens and androgens. 1129 63


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