Gene expression of 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase in relation to androstenone, testosterone, and estrone sulphate in gonadally intact male and castrated pigs1

2007 ◽  
Vol 85 (10) ◽  
pp. 2457-2463 ◽  
Author(s):  
G. Chen ◽  
E. Bourneuf ◽  
S. Marklund ◽  
G. Zamaratskaia ◽  
A. Madej ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hydroxysteroid Dehydrogenase ◽  
Intact Male ◽  
Estrone Sulphate

Androgen regulation and site specificity of angiotensinogen gene expression and secretion in rat adipocytes

2000 ◽  
Vol 279 (6) ◽  
pp. E1398-E1405 ◽  
Author(s):  
Valérie Serazin-Leroy ◽  
Mireille Morot ◽  
Philippe de Mazancourt ◽  
Yves Giudicelli
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Protein Secretion ◽  
Male Rats ◽  
Fat Cells ◽  
Intact Male ◽  
Rat Adipocytes ◽  
Fat Deposits

Adipose tissue is an important source of angiotensinogen (ATG), and hypertension is commonly associated with android obesity. Therefore, we tested the hypothesis that androgens may control ATG gene expression and secretion in rat fat cells. In intact male rats, ATG mRNA expression (Northern blot and co-reverse transcription-polymerase chain reaction analysis) and protein secretion were significantly higher in deep intra-abdominal (perirenal and epididymal) than in subcutaneous adipocytes. After castration, ATG mRNA was reduced almost 50% in the three fat deposits, with parallel changes in ATG protein secretion. Conversely, testosterone treatment fully restored the ATG mRNA decrease after castration, whatever the anatomical origin of the adipocytes. Finally, a 24-h in vitro exposure of perirenal fat cells or differentiated preadipocytes from castrated rats to testosterone or dihydrotestosterone (10 nM free hormone concentration) increased ATG mRNA expression by 50–100%, an effect that was prevented by the anti-androgen cyproterone acetate. These data, demonstrating both in vivo and in vitro androgen induction of ATG mRNA expression in rat adipocytes, add further weight to the hypothesis of a link between adipose tissue ATG production, androgens, and android obesity-related hypertension.

DEFECTIVE STEROIDAL SYNTHESIS BY ADRENAL TISSUE: THE CONTROL OF GENE EXPRESSION CAUSING LOSS OF ACTIVE STEROIDOGENIC ENZYMES

1974 ◽  
Vol 77 (2) ◽  
pp. 325-336
Author(s):  
K. Williams
Keyword(s):  
Gene Expression ◽  
Adrenal Glands ◽  
Hydroxysteroid Dehydrogenase ◽  
Ascites Cell ◽  
Control Of Gene Expression ◽  
Adrenocortical Hyperplasia ◽  
Normal Human ◽  
Adrenocortical Tumour

ABSTRACT RNA was isolated from normal human adrenal glands and found to cause the formation of Δ5-3β-hydroxysteroid dehydrogenase-isomerase and steroid 21-hydroxylase activities by a Krebs II ascites cell-free protein synthesising system. Although no functional steroid 21-hydroxylase in vivo or in vitro was found in a gland from a patient with virilism due to congenital adrenocortical hyperplasia the RNA would still give steroid 21-hydroxylase-like activity in the protein synthesising system which suggests that the inherited defect was not in the structural gene. Activity could not be induced by RNA from a 'non-functioning' adrenocortical tumour or rat liver.

scholarly journals Course of placental 11beta-hydroxysteroid dehydrogenase type 2 and 15-hydroxyprostaglandin dehydrogenase mRNA expression during human gestation

2001 ◽  
pp. 187-192 ◽  
Author(s):  
E Schoof ◽  
M Girstl ◽  
W Frobenius ◽  
M Kirschbaum ◽  
R Repp ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Placental Tissue ◽  
Hydroxysteroid Dehydrogenase ◽  
Normal Pregnancy ◽  
Premature Babies ◽  
Gene Level ◽  
Human Placental Tissue ◽  
Human Placental Cells

BACKGROUND: During human pregnancy, 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays an important role in protecting the fetus from high maternal glucocorticoid concentrations by converting cortisol to inactive cortisone. Furthermore, 11beta-HSD2 is indirectly involved in the regulation of the prostaglandin inactivating enzyme 15-hydroxyprostaglandin dehydrogenase (PGDH), because cortisol reduces the gene expression and enzyme activity of PGDH in human placental cells. OBJECTIVE: To examine developmental changes in placental 11beta-HSD2 and PGDH gene expression during the 2nd and 3rd trimesters of human pregnancies. METHODS: In placental tissue taken from 20 healthy women with normal pregnancy and 20 placentas of 17 mothers giving birth to premature babies, 11beta-HSD2 and PGDH mRNA expression was determined using quantitative real-time PCR. RESULTS: Placental mRNA expression of 11beta-HSD2 and PGDH increased significantly with gestational age (r=0.55, P=0.0002 and r=0.42, P=0.007). In addition, there was a significant correlation between the two enzymes (r=0.58, P<0.0001). CONCLUSIONS: In the course of pregnancy there is an increase in 11beta-HSD2 and PGDH mRNA expression in human placental tissue. This adaptation of 11beta-HSD2 prevents increasing maternal cortisol concentrations from transplacental passage and is exerted at the gene level. 11beta-HSD2 up-regulation may also lead to an increase in PGDH mRNA concentrations that, until term, possibly delays myometrial contractions induced by prostaglandins.

scholarly journals Enhancement of Cortisol-Induced 11β-Hydroxysteroid dehydrogenase Type 1 Expression by Interleukin 1β in Cultured Human Chorionic Trophoblast Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (5) ◽  
pp. 2490-2495 ◽  
Author(s):  
Wenjiao Li ◽  
Lu Gao ◽  
Yan Wang ◽  
Tao Duan ◽  
Leslie Myatt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Phospholipase A2 ◽  
Mrna Expression ◽  
Reporter Gene ◽  
Reductase Activity ◽  
Hydroxysteroid Dehydrogenase ◽  
Cytosolic Phospholipase A2 ◽  
Trophoblast Cells ◽  
Cytosolic Phospholipase

Chorion is the most abundant site of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) expression within intrauterine tissues. It is important to study the regulation of 11β-HSD1 expression in the chorion in terms of local cortisol production during pregnancy. Using real-time PCR and enzyme activity assay, we found that cortisol (1 μm) and IL-1β (10 ng/ml) for 24 h significantly increased 11β-HSD1 mRNA expression and reductase activity in cultured human chorionic trophoblasts. A further significant increase of 11β-HSD1 mRNA expression and reductase activity was observed with cotreatment of cortisol and IL-1β. To explore the mechanism of induction, 11β-HSD1 promoter was cloned into pGL3 plasmid expressing a luciferase reporter gene. By transfecting the constructed vector into WISH cells, an amnion-derived cell line, we found that cortisol (1 μm) or IL-1β (10 ng/ml) significantly increased reporter gene expression. Likewise, an additional increase in reporter gene expression was observed with cotreatment of cortisol and IL-β. To explore the physiological significance of 11β-HSD1 induction in the chorion, we studied the effect of cortisol on cytosolic phospholipase A2 and cyclooxygenase 2 expression. We found that treatment of chorionic trophoblast cells with cortisol (1 μm) induced both cytosolic phospholipase A2 and cyclooxygenase 2 mRNA expression. We conclude that cortisol up-regulates 11β-HSD1 expression through induction of promoter activity, and the effect was enhanced by IL-1β, suggesting that more biologically active glucocorticoids could be generated in the fetal membranes in the presence of infection, which may consequently feed forward in up-regulation of prostaglandin synthesis.

scholarly journals Expression of Stress-Mediating Genes is Increased in Term Placentas of Women with Chronic Self-Perceived Anxiety and Depression

Genes ◽  
2020 ◽  
Vol 11 (8) ◽  
pp. 869
Author(s):  
Cristina A. Martinez ◽  
Ina Marteinsdottir ◽  
Ann Josefsson ◽  
Gunilla Sydsjö ◽  
Elvar Theodorsson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Depression Scale ◽  
Hydroxysteroid Dehydrogenase ◽  
Control Group ◽  
Stress Biomarkers ◽  
Index Group ◽  
Pregnancy And Delivery ◽  
Glcnac Transferase ◽  
Offspring Gender ◽  
Cutoff Threshold

Anxiety, chronical stress, and depression during pregnancy are considered to affect the offspring, presumably through placental dysregulation. We have studied the term placentae of pregnancies clinically monitored with the Beck’s Anxiety Inventory (BAI) and Edinburgh Postnatal Depression Scale (EPDS). A cutoff threshold for BAI/EPDS of 10 classed patients into an Index group (>10, n = 23) and a Control group (<10, n = 23). Cortisol concentrations in hair (HCC) were periodically monitored throughout pregnancy and delivery. Expression differences of main glucocorticoid pathway genes, i.e., corticotropin-releasing hormone (CRH), 11β-hydroxysteroid dehydrogenase (HSD11B2), glucocorticoid receptor (NR3C1), as well as other key stress biomarkers (Arginine Vasopressin, AVP and O-GlcNAc transferase, OGT) were explored in medial placentae using real-time qPCR and Western blotting. Moreover, gene expression changes were considered for their association with HCC, offspring, gender, and birthweight. A significant dysregulation of gene expression for CRH, AVP, and HSD11B2 genes was seen in the Index group, compared to controls, while OGT and NR3C1 expression remained similar between groups. Placental gene expression of the stress-modulating enzyme 11β-hydroxysteroid dehydrogenase (HSD11B2) was related to both hair cortisol levels (Rho = 0.54; p < 0.01) and the sex of the newborn in pregnancies perceived as stressful (Index, p < 0.05). Gene expression of CRH correlated with both AVP (Rho = 0.79; p < 0.001) and HSD11B2 (Rho = 0.45; p < 0.03), and also between AVP with both HSD11B2 (Rho = 0.6; p < 0.005) and NR3C1 (Rho = 0.56; p < 0.03) in the Control group but not in the Index group; suggesting a possible loss of interaction in the mechanisms of action of these genes under stress circumstances during pregnancy.

scholarly journals 17β-Hydroxysteroid Dehydrogenase Type 1, 2, 3, and 4 Expression and Enzyme Activity in Human Anterior Pituitary Adenomas

1999 ◽  
Vol 84 (4) ◽  
pp. 1340-1345
Author(s):  
V. L. Green ◽  
V. Speirs ◽  
A. M. Landolt ◽  
P. M. Foy ◽  
S. L. Atkin
Keyword(s):  
Gene Expression ◽  
Enzyme Activity ◽  
Pituitary Adenomas ◽  
Anterior Pituitary ◽  
Estrogenic Activity ◽  
Hydroxysteroid Dehydrogenase ◽  
Messenger Ribonucleic Acid ◽  
Human Anterior Pituitary

17β-Hydroxysteroid dehydrogenase (17βHSD) isoforms reversibly catalyze the final step in the formation of estradiol (E2) from estrone (E1) and the formation of testosterone from androstenedione. We have investigated 17βHSD type 1, 2, 3, and 4 gene expression and 17βHSD estrogenic activity in human anterior pituitary adenomas. 17βHSD messenger ribonucleic acid (mRNA) expression was studied by RT-PCR in 42 pituitary tumors and 3 normal pituitaries, 17βHSD activity was studied in 11 tumors and 17βHSD type 1 was immunolocalized in vitro in 6 tumors. 17βHSD type 1 gene expression was detected in 34 of 42 adenomas in all tumor subtypes; 17βHSD type 2 mRNA was detected in 18 of 42 adenomas, but not in prolactinomas; 17βHSD type 3 mRNA was detected in 12 of 42 adenomas, but not in corticotropinomas; 17βHSD type 4 was expressed in 20 of 42 adenomas by all adenoma subtypes. Reversible 17βHSD activity was found in 9 of 11 adenomas, and 17βHSD type 1 immunopositivity was cytoplasmically distributed in all 6 adenomas in vitro. All 4 17βHSD isoforms are variably expressed in human anterior pituitary adenomas, which also show 17βHSD enzyme activity, suggesting that 17βHSD may play an important role in regulating the local cellular levels of estradiol.

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