11β-Hydroxysteroid dehydrogenase and the pre-receptor regulation of corticosteroid hormone action

Draper, Norman R.; Stewart, Paul M.

doi:10.1677/joe.1.06019

Cited by 346 publications

(308 citation statements)

References 176 publications

(104 reference statements)

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“…Neurosecretory cells, as well as metabolic tissues such as liver and adipose tissue express the NADPHdependent 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1), which is the major determinant and limiting factor controlling GC concentration and their access to their cognate receptors in target cells [77,78] . 11β-HSD1 has been localized in the mouse and rat hippocampus, hypothalamus, and pituitary, demonstrating its importance in the negative feedback regulation of endogenous GCs within the HPA axis.…”

Section: Glucocorticoidsmentioning

confidence: 99%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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Abnormal function of the hypothalamic-pituitary-adrenal (HPA) axis is an important pathological finding in pregnant women exhibiting major depressive disorder. They show high levels of cortisol proinflammatory cytokines, hypothalamic-pituitary peptide hormones and catecholamines, along with low dehydroepiandrosterone levels in plasma. During pregnancy, the TH2 balance together with the immune system and placental factors play crucial roles in the development of the fetal allograft to full term. These factors, when altered, may generate a persistent dysfunction of the HPA axis that may lead to an overt transfer of cortisol and toxicity to the fetus at the expense of reduced activity of placental 11β-hydroxysteroid dehydrogenase type 2. Epigenetic modifications also may contribute to the dysregulation of the HPA axis. Affective disorders in pregnant women should be taken seriously, and therapies focused on preventing the deleterious effects of stressors should be implemented to promote the welfare of both mother and baby.Keywords: brain; depression; neuroendocrine; pregnancy; stress; glucocorticoids Extensive studies have demonstrated that early life stressors produce changes in behavior and enhance the sensitivity of the stress response systems [1][2][3][4] . Although the genetic background has been implicated in the development of mood-related disorders, and genetic research has identified some chromosomal regions and genes that are involved in susceptibility to mood disorders, the etiology of anxiety and depressive disorders is still not clear in humans, particularly in women with major depressive disorder (MDD) [1] .The pathogenesis of perinatal depression is an emerging field. Although considerable progress has been made in this area in the last few years, there still remain unanswered questions and gaps in our knowledge of the underlying pathogenesis, the long-term impact of perinatal depression on the developing fetus, and the best methods for counseling pregnant women concerning the risks of untreated MDD versus the risks of psychopharmacologic treatment during pregnancy and lactation [5] . Meta-analysis studies have reported that the mean prevalence rate of prenatal depression is ~12% (this varies greatly according to location, mode of assessment, and socioeconomic conditions), and show that a large percentage of pregnant women displaying major depression remain depressed in the postpartum period and/or continuously [6,7] . Anxiety, depressive disorder, and stress during pregnancy are risk Phillipe Leff Gelman, et al. HPA axis in perinatal depression 339 factors for negative outcomes in newborns, like preterm birth or low birth weight; also, insecure attachment and impaired child development could be a consequence of mental disorders during pregnancy [6,[8][9][10] . The mechanisms by which maternal depression impacts fetal and neonatal development are currently under investigation; there is some evidence that depressive symptoms impact the infant's hypothalamic-pituitary-adrenal (HPA) axis, enhancing the ...

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Section: Glucocorticoidsmentioning

confidence: 99%

Hypothalamic-pituitary-adrenal axis function during perinatal depression

et al. 2015

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“…Tissue specific reactions are explained by the levels of circulating cortisol and the degree of expression of the cortisol receptor. More recently, research was focussed on the 11ß-hydroxysteroid-dehydrogenase enzymes (11ß-HSD), which play a role in the pre-receptor regulation of glucocorticoid hormone action (for review see Draper and Stewart, 2005). Two isoforms were characterized: 11ß-HSD2 is a unidirectional high affinity enzyme which oxidizes active cortisol to inactive cortisone in the presence of NAD + as a cofactor (Albiston et al, 1994;Brown et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…in the brain of perinatal rats, is similarly regarded to protect the brain against disturbances of glucocorticoid-dependent programming of behavior later in life (Holmes and Seckl, 2006). A possible role for tumorigenesis was also reported due to the antiproliferative effects of glucocorticoids (Rogatsky et al, 1997) which are reduced by an increased 11ß-HSD2 expression in a number of tumors (see: Draper and Stewart, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Expression of 11β-hydroxysteroid-dehydrogenase 2 in Sertoli cells of boar testes

Claus

Lacorn

Welter

et al. 2007

Molecular and Cellular Endocrinology

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Abstract11ß-hydroxysteroid dehydrogenase 2 (11ß-HSD2) activity occurs in boar testes but it is not known which cell types express 11ß-HSD2 mRNA and protein. Therefore, testes samples were taken from mature boars. For immunocytochemistry and Western Blot pig specific antibodies were raised against a 10 amino acid peptide corresponding to amino acids 391-400 of the coding sequence. Quantitative PCR was performed in testis homogenates and additionally RT-PCR in samples collected by UV-single cell microdissection. Data show that in interstitial tissue 11ß-HSD2 is expressed in Leydig cells and additionally in blood capillaries. In tubuli, 11ß-HSD2 primarily is formed in Sertoli cells whereas occurrence in spermatogonia could not be definitely proven. Because glucocorticoid receptors were never found in boar Leydig cells it is concluded that the expression of 11ß-HSD2 in several types of cells forms consecutive lines of defense to protect spermatogonia against glucocorticoidinduced apoptosis.

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“…Many cells, including immune cells, express 11β-HSD1, which has the potential to dramatically influence local glucocorticoid availability, within individual cells and within tissues. 11β-HSD1, including its role in the inflammatory response, has been the subject of a number of recent reviews (eg (Chapman et al, 2006a;Chapman et al, 2006b;Chapman and Seckl, 2008;Draper and Stewart, 2005;Morton and Seckl, 2008;Oppermann, 2006;Seckl, 2004)). Hence, in this review we concentrate on recent data relevant to the role and regulation of 11β-HSD1 during inflammation.…”

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confidence: 99%