EC Number   |
General Information |
Reference |
|---|
   1.1.1.B40 | more |
species-specific differences of rat and human placental 11beta-HSD2 steroid turnover, species-specific expression of corticotropin-releasing hormone and steroids in human and rat term placenta |
-, 743434 |
| 1.1.1.B40 | physiological function |
11beta-hydroxysteroid dehydrogenase type 1 (11HSD1) is an enzyme that regulates the conversion of glucocorticoids from inactive to active form. Expression of expression of glucocorticoid and mineralocorticoid receptors and 11beta-hydroxysteroid dehydrogenase type 1 determines the sensitivity of the hippocampus to glucocorticoids, which mediate the feedbac inhibition of the hypothalamus-pituitary-adrenal axis during stress response via the hippocampus. Depending on the strain, stress stimulates 11HSD1 in the ventral hippocampus, which is known to be involved in stress and emotion reactions whereas independent of strain, stress inhibits the glucorticoid receptor in the dorsal hippocampus, which is predominantly involved in cognitive functions. F344 rats may amplify the hippocampal glucocorticoid signal more effectively than the stressed Wistar and Lewis rats, or the positive effect of stressful stimuli on 11HSD1 requires a longer stress exposure in the Wistar and Lewis Rattus strains |
743428 |
| 1.1.1.B40 | physiological function |
the action of cortisol on the human feto-placental unit is regulated by 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2/HSD11B2) that converts cortisol into inactive cortisone. The mRNA expression of HSD11B2 correlates with indirect and direct cortisol turnover rates in C-section placentas only. In contrast to C-sections, corticotropin-releasing hormone, cortisol and cortisone levels are significantly increased in placental samples following spontaneous birth |
760443 |
| 1.1.1.B40 | physiological function |
the enzyme plays a key role in fetal development. p38 MAPK is a positive regulator of placental 11beta-HSD2, p38 MAPK upregulates placental 11b-HSD2 by increasing the half-life of 11beta-HSD2 mRNA. Also ERK1/2 signaling is involved in regulation of placental 11beta-HSD2, ERK1/2 inhibitor U0126 induces the enzyme expression in trophoblasts. siRNA-mediated knockdown of ERK1/2 expression leads to a similar increase in levels of 11beta-HSD2 protein, as seen in cells treated with the ERK1/2 pharmacological inhibitor |
742040 |
| 1.1.1.B40 | physiological function |
the placenta acts as a master regulator for the fetal environment, mediating intrauterine exposures to stress through the activity of genes regulating glucocorticoids, including the 11beta-hydroxysteroid dehydrogenase (HSD11B) type 1 and 2 genes, variation in the genes are associated with infant birth weight. A significant association between methylation at a single CpG site within HSD11B1 and being born large for gestational age is detected. Correlations between methylation and gene expression. Methylation at a single CpG site within HSD11B1 is associated with infant birth weight, and that methylation at several different sites is correlated with gene expression. There is no sex-specific role of methylation in infant birth weight in either time points in pregnancy |
742042 |
| 1.1.1.B40 | physiological function |
the placenta acts as a master regulator for the fetal environment, mediating intrauterine exposures to stress through the activity of genes regulating glucocorticoids, including the 11beta-hydroxysteroid dehydrogenase (HSD11B) type 1 and 2 genes, variation in the genes are associated with infant birth weight. Correlations between methylation and gene expression, including sex-specific transcriptional regulation of HSD11B2 |
742042 |
| 1.1.1.B40 | physiological function |
the placental enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11b-HSD2) shields the fetus from maternal glucocorticoid excess by catalyzing the conversion of these hormones into biologically inactive derivatives |
743434 |
| 1.1.1.B40 | physiological function |
the placental enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) shields the fetus from maternal glucocorticoid excess by catalyzing the conversion of these hormones into biologically inactive derivatives |
-, 743434 |
