Testicular 3β-hydroxysteroid dehydrogenase/Δ5–4 isomerase in the hypophysectomized rat: effect of treatment with 5α-dihydrotestosterone

Fanjul, Luisa F.; Quintana, José; Gonzalez, J. E.; Santana, Pino; Estévez, Francisco; Galarreta, C. M. Ruiz de

doi:10.1677/joe.0.1330237

Cited by 8 publications

(4 citation statements)

References 34 publications

(49 reference statements)

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“…BMP-4, -6 and -7 also lower basal HSD3B mRNA in theca cells (109). Numerous other hormones and growth factors negatively impact 3b-HSD protein levels or enzymatic activity in gonadal cells including glucocorticoids (328)(329)(330)(331), but their effects on HSD3B mRNA are not characterized.…”

Section: Hormonal Control Of Hsd3b Gene Expressionmentioning

confidence: 97%

Transcriptional Regulation of Steroidogenic Genes: STARD1, CYP11A1 and HSD3B

LaVoie

King

2009

Exp Biol Med (Maywood)

219

159

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Expression of the genes that mediate the first steps in steroidogenesis, the steroidogenic acute regulatory protein (STARD1), the cholesterol side-chain cleavage enzyme, cytochrome P450scc (CYP11A1) and 3beta-hydroxysteroid dehydrogenase/Delta5-Delta4 isomerase (HSD3B), is tightly controlled by a battery of transcription factors in the adrenal cortex, the gonads and the placenta. These genes generally respond to the same hormones that stimulate steroid production through common pathways such as cAMP signaling and common actions on their promoters by proteins such as NR5A and GATA family members. However, there are distinct temporal, tissue and species-specific differences in expression between the genes that are defined by combinatorial regulation and unique promoter elements. This review will provide an overview of the hormonal and transcriptional regulation of the STARD1, CYP11A1 and specific steroidogenic HSD3B genes in the adrenal, testis, ovary and placenta and discuss the current knowledge regarding the key transcriptional factors involved.

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Section: Hormonal Control Of Hsd3b Gene Expressionmentioning

confidence: 97%

Transcriptional Regulation of Steroidogenic Genes: STARD1, CYP11A1 and HSD3B

LaVoie

King

2009

Exp Biol Med (Maywood)

219

159

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“…Rats treated with hCG showed an increase in 3␤-HSD activity, but R1881 (androgen agonist) decreased hCG induction, whereas cyproterone acetate (androgen antagonist) increased activity (405). Similarly, DHT and methyltrienolone (androgen agonist) inhibited 3␤-HSD activity in adult rat Leydig cells (409), and T decreased 3␤-HSD activity in Leydig cells from C57BL/6J mice (134, 410). Disruption of steroidogenesis with aminoglutethimide (AMG) treatment increased 3␤-HSD and P450c17 mRNA levels, whereas treatment with T and cAMP reversed this effect (411).…”

Section: Steroidsmentioning

confidence: 99%

Molecular Biology of the 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4 Isomerase Gene Family

et al. 2005

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The 3beta-hydroxysteroid dehydrogenase/Delta(5)-Delta(4) isomerase (3beta-HSD) isoenzymes are responsible for the oxidation and isomerization of Delta(5)-3beta-hydroxysteroid precursors into Delta(4)-ketosteroids, thus catalyzing an essential step in the formation of all classes of active steroid hormones. In humans, expression of the type I isoenzyme accounts for the 3beta-HSD activity found in placenta and peripheral tissues, whereas the type II 3beta-HSD isoenzyme is predominantly expressed in the adrenal gland, ovary, and testis, and its deficiency is responsible for a rare form of congenital adrenal hyperplasia. Phylogeny analyses of the 3beta-HSD gene family strongly suggest that the need for different 3beta-HSD genes occurred very late in mammals, with subsequent evolution in a similar manner in other lineages. Therefore, to a large extent, the 3beta-HSD gene family should have evolved to facilitate differential patterns of tissue- and cell-specific expression and regulation involving multiple signal transduction pathways, which are activated by several growth factors, steroids, and cytokines. Recent studies indicate that HSD3B2 gene regulation involves the orphan nuclear receptors steroidogenic factor-1 and dosage-sensitive sex reversal adrenal hypoplasia congenita critical region on the X chromosome gene 1 (DAX-1). Other findings suggest a potential regulatory role for STAT5 and STAT6 in transcriptional activation of HSD3B2 promoter. It was shown that epidermal growth factor (EGF) requires intact STAT5; on the other hand IL-4 induces HSD3B1 gene expression, along with IL-13, through STAT 6 activation. However, evidence suggests that multiple signal transduction pathways are involved in IL-4 mediated HSD3B1 gene expression. Indeed, a better understanding of the transcriptional factors responsible for the fine control of 3beta-HSD gene expression may provide insight into mechanisms involved in the functional cooperation between STATs and nuclear receptors as well as their potential interaction with other signaling transduction pathways such as GATA proteins. Finally, the elucidation of the molecular basis of 3beta-HSD deficiency has highlighted the fact that mutations in the HSD3B2 gene can result in a wide spectrum of molecular repercussions, which are associated with the different phenotypic manifestations of classical 3beta-HSD deficiency and also provide valuable information concerning the structure-function relationships of the 3beta-HSD superfamily. Furthermore, several recent studies using type I and type II purified enzymes have elegantly further characterized structure-function relationships responsible for kinetic differences and coenzyme specificity.

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“…Galarreta et al [40] and Tanaka et al [41] noted that P 4 downregulates the activity of 3βHSD in rat ovaries. Feedback regulation of 3βHSD under the impact of androgens was also observed in the rat testicular Leydig cells [42,43]. Differences in the effect of chemerin on enzyme protein abundance and steroid production may additionally result from the ability of both P 4 and E 2 to convert into the other hormones in the subsequent stages of the steroidogenesis process [31].…”

Section: Discussionmentioning

confidence: 79%

Chemerin Affects P4 and E2 Synthesis in the Porcine Endometrium during Early Pregnancy

Gudelska

Dobrzyń

Kieżun

et al. 2022

IJMS

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Chemerin, belonging to the adipokine family, exhibits pleiotropic activity. We hypothesised that the adipokine could be involved in the regulation of steroidogenesis in the porcine endometrium. Thus, the aim of this study was to determine the effect of chemerin on the key steroidogenic enzyme proteins’ abundance (Western blot), as well as on P4 and E2 secretion (radioimmunoassay) by the porcine endometrium during early pregnancy and the mid-luteal phase of the oestrous cycle. Moreover, we investigated the hormone impact on Erk and Akt signalling pathway activation (Western blot). Chemerin stimulated E2 production on days 10 to 11 of pregnancy. On days 10 to 11 and 15 to 16 of gestation, and on days 10 to 11 of the cycle, chemerin enhanced the expression of StAR and all steroidogenic enzyme proteins. On days 12 to 13 of pregnancy, chemerin decreased StAR and most of the steroidogenic enzyme proteins’ abundance, whereas the P450C17 abundance was increased. On days 27 to 28 of pregnancy, chemerin increased StAR and P450C17 protein contents and decreased 3βHSD protein amounts. It was noted that the adipokine inhibited Erk1/2 and stimulated Akt phosphorylation. The obtained results indicate that chemerin affected P4 and E2 synthesis through the Erk1/2 and Akt signalling pathways.

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Testicular 3β-hydroxysteroid dehydrogenase/Δ5–4 isomerase in the hypophysectomized rat: effect of treatment with 5α-dihydrotestosterone

Cited by 8 publications

References 34 publications

Transcriptional Regulation of Steroidogenic Genes: STARD1, CYP11A1 and HSD3B

Transcriptional Regulation of Steroidogenic Genes: STARD1, CYP11A1 and HSD3B

Molecular Biology of the 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4 Isomerase Gene Family

Chemerin Affects P4 and E2 Synthesis in the Porcine Endometrium during Early Pregnancy

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