Catabolism and interconversion of cortisol and cortisone in human synovial tissue in vitro.

Dl, Murphy; West, H. F.

doi:10.1136/ard.28.6.637

Cited by 10 publications

(11 citation statements)

References 10 publications

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“…Therefore, it would be preferable to use Nunc Maxicorp plates. Nonetheless, these results confirm that ϳ50% of serum and CSF samples contain antibodies to HSA (and presumably to BSA as well, since it was previously shown that all sera positive for anti-HSA contained antibodies to BSA [4]). …”

supporting

confidence: 86%

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Cortisol metabolism by 11β‐hydroxysteroid dehydrogenase as a novel target in the treatment of inflammation‐ or immune‐mediated bone loss: Comment on the article by Makrygiannakis et al

Wilckens¹,

Volkmann²

2007

Arthritis & Rheumatism

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supporting

confidence: 86%

“…The shuttle is present at sites of inflammation (ref. 4 and Volkmann A, Wilckens T: unpublished observations) and also in bone (5). It is intriguing that patients with early RA show transient expression of the catabolizing enzyme in monocytes during the first 2 years of disease (6).…”

Section: To the Editormentioning

confidence: 89%

Cortisol metabolism by 11β‐hydroxysteroid dehydrogenase as a novel target in the treatment of inflammation‐ or immune‐mediated bone loss: Comment on the article by Makrygiannakis et al

Wilckens¹,

Volkmann²

2007

Arthritis & Rheumatism

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“…Relatively soon after the introduction of cortisone and cortisol (hydrocortisone) as treatments for RA, it became clear that inflamed synovial tissue was capable of interconverting these two glucocorticoids . Original hypotheses that synovial tissue might break down glucocorticoids in RA, thus leaving the joint deficient in steroids, were not supported by these early data that demonstrated that at least some cortisone could be converted to cortisol . A renewal of interest in this area occurred following the development of refined techniques for the study of glucocorticoid metabolism and the molecular characterization of the two distinct 11β‐HSD enzymes.…”

Section: Glucocorticoid Metabolism In Synovial Tissuementioning

confidence: 99%

Glucocorticoid metabolism in rheumatoid arthritis

Hardy

Raza

Cooper

2014

Annals of the New York Academy of Sciences

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Endogenous glucocorticoids are implicated in the development and resolution of inflammation. Until recently it was thought that these glucocorticoids arose primarily from the adrenal gland. However, it is now known that several cell types can generate active glucocorticoids within their cytoplasm through expression of the 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme. In a more limited range of cell types, glucocorticoids can be inactivated by the related 11β-HSD2 enzyme. Both enzymes are regulated by inflammation in various settings. In rheumatoid arthritis, 11β-HSD activity is present in the inflamed synovium and appears to influence articular and extraarticular disease processes. The generation of active glucocorticoids in the synovium is strongly linked to the level of inflammation. This local production of glucocorticoids is likely to have paracrine consequences and could underpin inflammation-associated bone loss. The role of 11β-HSD enzymes in the severity and persistence of inflammatory arthritis in a clinical setting is currently being explored.

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“…In the late 1960s, a role for peripheral cortisone-cortisol interconversion in RA was described [2] and involvement of synovial tissue in this interconversion was shown [3]. However, more detailed elucidation of the underlying mechanisms was possible only after the necessary techniques became available [4].…”

Section: Introductionmentioning

confidence: 99%

11β-Hydroxysteroid Dehydrogenase Enzymes Modulate Effects of Glucocorticoids in Rheumatoid Arthritis Synovial Cells

Schmidt

Straub

2014

Neuroimmunomodulation

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The tissue availability of active glucocorticoids (cortisol in humans) depends on their rate of synthesis from cholesterol, downstream metabolism, excretion and interconversion. The latter is mediated by the 11β-hydroxysteroid dehydrogenases (11βHSDs). In this review, we summarize the features of the two isoenzymes, 11βHSD1 and 11βHSD2, and current available experimental data related to 11βHSDs, which are relevant in the context of synovial cells in rheumatoid arthritis (RA). We conclude that due to complex feedback mechanisms inherent to the hypothalamic-pituitary-adrenal axis, currently available transgenic animal models cannot display the full potential otherwise inherent to the techniques. Studies with tissue explants, mixed synovial cell preparations, cell lines derived from synovial cells, and related primary cells or established cell lines indicate that there are relatively clear differences between the two isoenzymes. 11βHSD1 is expressed primarily in fibroblasts and osteoblasts, and may be responsible for fibroblast survival and aid in the resolution of inflammation, but it is also involved in bone damage. 11βHSD2 is expressed primarily in macrophages and lymphocytes, and may be responsible for their survival, suggesting that it is critical in chronic inflammation. The situation in synovial tissue would allow 11βHSD2-expressing cells to tap the energy resources of 11βHSD1-expressing cells. The overall properties of this local glucocorticoid interconversion system might limit therapeutic use of glucocorticoids in RA.

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Catabolism and interconversion of cortisol and cortisone in human synovial tissue in vitro.

Cited by 10 publications

References 10 publications

Cortisol metabolism by 11β‐hydroxysteroid dehydrogenase as a novel target in the treatment of inflammation‐ or immune‐mediated bone loss: Comment on the article by Makrygiannakis et al

Cortisol metabolism by 11β‐hydroxysteroid dehydrogenase as a novel target in the treatment of inflammation‐ or immune‐mediated bone loss: Comment on the article by Makrygiannakis et al

Glucocorticoid metabolism in rheumatoid arthritis

11β-Hydroxysteroid Dehydrogenase Enzymes Modulate Effects of Glucocorticoids in Rheumatoid Arthritis Synovial Cells

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