11β-Hydroxysteroid Dehydrogenase Type 2 in Human Lung: Possible Regulator of Mineralocorticoid Action

Suzuki, Takashi; Sasano, Hironobu; Suzuki, Satoshi; Hirasawa, Gen; Takeyama, Junji; Muramatsu, Yasunari; Date, Fumiko; Nishimura, Hiroshi; Krozowski, Zygmunt

doi:10.1210/jcem.83.11.5227

Cited by 32 publications

(31 citation statements)

References 28 publications

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“…11b-HSD-type2 is also detected in human lung epithelia and in epithelia of the trachea and bronchioli, where it seems to be co-localized with MR and may play a role in sodium and fluid transport of the airway epithelia, especially in the fetus (53).…”

Section: B-hsd-type1mentioning

confidence: 97%

Clinical implications of glucocorticoid metabolism by 11beta-hydroxysteroid dehydrogenases in target tissues

Quinkler

Oelkers²,

Diederich³

2001

European Journal of Endocrinology

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11b-Hydroxysteroid dehydrogenases (11b-HSD) are microsomal enzymes that catalyze the conversion of active glucocorticoids (GC) to their inactive 11-dehydro products and vice versa. Two isoenzymes of 11b-HSD have been characterized and cloned in human tissues. The tissue-specific metabolism of GC by these enzymes is important for mineralocorticoid (MC) and GC receptor occupancy and seems to play a crucial role in the pathogenesis of diseases such as apparent MC excess syndrome, and may play roles in hypertension, obesity and impaired hepatic glucose homeostasis. This article reviews the literature and examines the role and importance of 11b-HSD in humans.

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Section: B-hsd-type1mentioning

confidence: 97%

Clinical implications of glucocorticoid metabolism by 11beta-hydroxysteroid dehydrogenases in target tissues

Quinkler

Oelkers²,

Diederich³

2001

European Journal of Endocrinology

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“…HSD2 gene expression has been detected in human fetal lung via immunohistochemistry, RT-PCR, and immunoblot analyses (12,13). In contrast, HSD1 protein is undetectable in human adult and fetal lung tissues (12,21,22).…”

Section: Discussionmentioning

confidence: 99%

“…HSD2 mRNA and protein have been detected in human adult and fetal lung tissues, as well as in a number of human lung epithelial cell lines (12,13). In contrast, the oxidoreduction of cortisone to cortisol (suggestive of HSD1 activity) is negligible in intact cultured lung explants and undetectable in human fetal lung in vivo (11,14,15).…”

mentioning

confidence: 99%

11-β Hydroxysteroid Dehydrogenase Type 2 in Human Adult and Fetal Lung and Its Regulation by Sex Steroids

et al. 2007

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11-␤ hydroxysteroid dehydrogenase type 2 (HSD2) oxidizes the biologically active glucocorticoid (GC), cortisol, to inactive cortisone. We characterized HSD2 gene expression and activity in human adult and fetal lung tissues and in cultured fetal lung explants, and examined the potential regulation of HSD2 in the fetal lung by sex steroids. Human adult lung, fetal lung, and cultured fetal lung explant tissues contained similar amounts of HSD2 mRNA. However, higher levels of HSD2 protein were detected in human fetal lung tissue than in adult lung, with expression being restricted to a subset of epithelial cells in the fetal lung tissue. Differentiated fetal lung explants maintained in culture expressed higher levels of HSD2 protein and enzymatic activity than undifferentiated fetal lung tissues. Finally, HSD2 protein levels were decreased in male, but not female, fetal lung explants treated with 17-␤ estradiol. In contrast, 5-␣ dihydrotestosterone did not significantly affect HSD2 levels. These data indicate that HSD2 protein and activity levels increase in parallel with the differentiation of alveolar type II epithelial cells in vitro, and that HSD2 protein levels are regulated by 17-␤ estradiol in male fetal lung tissue. (Pediatr Res 62: 26-31, 2007)

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“…This may be explained by the observation that TNFa and IL-1b both increased the expression levels and reductase activity of 11b-HSD-1 in a cell line in vitro [191]. However, the relative increase in reductase activity could also be due to a decrease in the activity of 11bHSD-2, since it has recently become apparent that this enzyme is present in lung [192]. Further enzymological and quantitative RT-PCR studies are required.…”

Section: Adrenal Steroids In Tuberculosismentioning

confidence: 99%

M. tuberculosis: immunology and vaccination

2001

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Tuberculosis is increasing. Current treatment regimens require at least 6 months, because latent or stationary phase organisms are difficult to kill. Such regimens do not achieve full compliance, and "directly observed therapy short course" (DOTS) is having less impact than expected. This worrying situation is aggravated by coinfection with human immunodeficiency virus (HIV), and by the increase in drug-resistant strains.We need new insights that lead to more rapid therapies and immunotherapies, and more reliable vaccines.Recent insights have come from: understanding of the relationship between Mycobacterium tuberculosis and macrophages; the multiple T cell types that recognise mycobacterial peptides, lipids and glycolipids; the critical role of interferon-c (IFNc) and interleukin-12 (IL-12) in human mycobacterial infection revealed by genetically defective children; quantitation of the presence and importance of Th2 lymphocyte activation in human tuberculosis; the role of local conversion of inactive cortisone to active cortisol in the lesions; the recognition that some effective prophylactic vaccines also work as immumotherapeutics whereas others do not. In the longer term the recent sequencing of the M. tuberculosis genome will lead to further advances.In the short term, effective immunotherapy remains the most accessible breakthrough in the management of tuberculosis. The types of practical advance that will result from sequencing the genome are discussed speculatively, but cannot yet be predicted with certainty.

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11β-Hydroxysteroid Dehydrogenase Type 2 in Human Lung: Possible Regulator of Mineralocorticoid Action

Cited by 32 publications

References 28 publications

Clinical implications of glucocorticoid metabolism by 11beta-hydroxysteroid dehydrogenases in target tissues

Clinical implications of glucocorticoid metabolism by 11beta-hydroxysteroid dehydrogenases in target tissues

11-β Hydroxysteroid Dehydrogenase Type 2 in Human Adult and Fetal Lung and Its Regulation by Sex Steroids

M. tuberculosis: immunology and vaccination

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