High impact information on 3B-HSD

• The present data indicate that activation of the protein kinase-C pathway induces generation of cAMP, but causes a near-complete inhibition of the stimulatory effects of hCG, LH, forskolin, cholera toxin, and cAMP analogs on 3 beta HSD mRNA levels in porcine granulosa cells in culture [1].
• In the same cell culture model, hCG induced a time-dependent increase in the 3 beta-hydroxy-5-ene steroid dehydrogenase (3 beta HSD) mRNA levels with a maximal 3-fold stimulation obtained at 8-16 h of incubation with 1 IU hCG/ml [1].
• The enzyme complex 3 beta-hydroxy-5-ene-steroid dehydrogenase/delta 5-delta 4-isomerase (3 beta HSD) is involved in the biosynthesis of all classes of active steroids, namely glucocorticoids, mineralocorticoids, progesterone, and sex hormone steroids [2].
• To obtain precise information about the cellular and subcellular localization of 3 beta HSD in the gonads and adrenals of the guinea pig, we have proceeded to immunocytochemical localization of the enzyme using antibodies developed against purified human placental 3 beta HSD [2].
• The present data suggest a functional interaction between the ovocyte and the specialized layer of 3 beta HSD-containing granulosa cells which might play a role in ovocyte maturation [2].

Biological context of 3B-HSD

• The 3 beta-HSD gene was mapped to the porcine chromosome 4q16-4q21 which is in accordance with the comparative gene map [3].
• An reverse-transcription-polymerase chain reaction (RT-PCR) probe from porcine testicular tissue of a 3 beta-HSD enzyme was used to screen a porcine adipose tissue cDNA library [3].
• Despite the increase in mRNA levels for 3 beta-HSD and P450c21, no increase in their respective enzyme activities was observed and 21-hydroxylase activity even declined over the 72-h incubation period with ACTH, thus suggesting that mechanism(s) other than gene expression alone regulate steroid secretion in FG cells [4].

Anatomical context of 3B-HSD

• The expression of 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) was localized to the theca interna and was unaffected by follicle atresia [5].
• Therefore, the steroidal regulation of 3 beta HSD in pig Leydig cells may act through a mechanism separate from the androgen receptor [6].
• In this study, we have examined the action of charcoal-treated and filtered follicular fluid on 3 beta-hydroxysteroid dehydrogenase activity (3 beta-HSD) and the ability of exogenous pregnenolone to increase progesterone secretion [7].
• The expression of 3 beta-HSD by porcine fetal testes was low compared with that of the fetal adrenal gland at all stages of development [8].
• Northern and Western analyses were performed to detect the cytochrome P450 enzyme 17 alpha-hydroxylase/17-20 lyase (P450c17) and that for cholesterol side-chain cleavage (P450scc), as well as 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) expression in several porcine fetal tissues [8].

Associations of 3B-HSD with chemical compounds

• PGF2 alpha interfered with LH and (bu)2cAMP induction of 3 beta-HSD and P450scc message, and this interference was dependent on the PGF2 alpha dose employed.(ABSTRACT TRUNCATED AT 250 WORDS)[9]
• In nonatretic follicles, increased follicle size was associated with a decrease (p < 0.01) in androgen receptor expression and increases (p < 0.01) in P450arom, P450c17, and 3 beta HSD expression [5].
• Treatment with hCG plus aminoglutethimide, an inhibitor of steroidogenesis, had no effect on the mRNA for the two P450 enzymes, but resulted in an increase in mRNA for 3 beta HSD when compared to treatment with hCG alone [6].
• The effects of prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) on the accumulation of progesterone and mRNA for the steroidogenic enzymes 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and cytochrome P450 side-chain cleavage (P450scc) were determined in luteinized granulosa cells [9].
• 3 beta-HSD was assayed by measuring the conversion of tritiated dehydroepiandrosterone (DHEA) to androstenedione in the presence of NAD+ [10].

Regulatory relationships of 3B-HSD

• Additionally, the activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) under the influence of GH added alone or together with IGF was measured by the conversion of pregnenolone to progesterone [11].

Other interactions of 3B-HSD

• The mRNA for IGF-I, IGF-II, IGFBP-2, LH receptor, FSH receptor, cytochrome P450 side-chain cleavage (P450scc), 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), 17 alpha-hydroxylase (P45017 alpha), and aromatase (P450arom) were detected by in situ hybridization, and relative amounts were determined by image analysis [12].
• Pig testicular 20 beta-hydroxysteroid dehydrogenase (20 beta-HSD) has also 3 alpha- and 3 beta-HSD (3 alpha/beta-HSD) activities [13].

Analytical, diagnostic and therapeutic context of 3B-HSD

• Cytochromes P450 17 alpha-hydroxylase/17-20 lyase (P450c17), aromatase (P450arom) and side-chain cleavage (P450scc), as well as 3 beta-hydroxysteroid dehydrogenase (3 beta HSD), were subjected to Northern and Western immunoblot analyses [14].
• Second, three steroidogenic enzymes, adrenodoxin, 17 alpha-hydroxylase-lyase (P450(17) alpha) and 3 beta-hydroxysteroid-dehydrogenase (3 beta-HSD) were detected by immunohistochemistry and quantified by image analysis on sections of the two largest follicles [15].
• The molecular weight was estimated to be 31 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and 28 kDa by gel filtration chromatography, indicating that the native 3 beta-HSD is a monomer [16].

References