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Fibroblast and Immune Cell Cross Talk in Cardiac Repair
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Stelios Psarras, Georgina Xanthou
There is evidence that neutrophil chemoattractants are overexpressed by cardiac fibroblasts in MI. Indeed, in mice lacking 11β-hydroxysteroid dehydrogenase type 1, CXCL2 and CXCL5 overexpression by cardiac fibroblasts was accompanied by increased neutrophilic inflammation (Figure 5.1), which was reversed by administration of corticosterone (38). Moreover, cardiac fibroblasts produce eotaxins (CCL11 and CCL24) and recruit eosinophils (Figure 5.1) in certain myocarditis conditions (39).
Late Effects of Treatment for Childhood Brain and Spinal Tumors
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Ralph Salloum, Katherine Baum, Melissa Gerstle, Helen Spoudeas, Susan R. Rose
Patients with ACTHD require daily hydrocortisone replacement, but not mineralocorticoid replacement, as this is produced by adrenal glands under the influence of renin-aldosterone (not ACTH). Hydrocortisone replacement therapy is 7–10 mg/m2 per day, divided into two or three oral doses. Dexamethasone is not used for replacement in children because it can suppress growth, but it can be used in doses of 0.25–0.5 mg once daily in adults. Adrenal crisis can develop with GH initiation, which is related to GH inhibiting 11β-hydroxysteroid dehydrogenase type 1 that converts cortisone to cortisol, or with levothyroxine initiation in unrecognized or undertreated ACTHD.45
Neuroprotective effects of food restriction in a rat model of traumatic brain injury – the role of glucocorticoid signaling
Published in Nutritional Neuroscience, 2022
Milka Perović, Milena Jović, Smilja Todorović, Aleksandra Mladenović Đorđević, Desanka Milanović, Selma Kanazir, Nataša Lončarević-Vasiljković
Since 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is the major regulator of the tissue-specific effects of circulating glucocorticoid excess, we next analyzed the protein level of this enzyme in the ipsilateral brain tissue (Figure 5). Two-way ANOVA with FR and time as factors revealed a significant effect of FR (F(1,40) = 15.243, p < 0.05), time (F(4,40) = 13.140, p < 0.05) and FR × time (F(4,40) = 9.544, p < 0.05) on 11β-HSD1 levels. They were significantly increased in AL group on the 2nd, 7th, 14th and 28th dpi (24%, 43%, 39%, and 37% respectively) compared to AL control (*p < 0.05). Oppositely, in the FR group, levels of 11β-HSD1 were significantly decreased on the 14th and 28th dpi (36% and 51%, respectively) compared to FR control (#p < 0.05). Post hoc analysis showed a significant decrease of 11β-HSD1 on the 2nd, 7th, 14th and 28th dpi in FR rats (28, 54, 75 and 88%, respectively) vs. AL rats at matching time points ($p < 0.05). However, WB analysis did not reveal any significant differences in 11β-HSD1 between AL and FR physiological controls.
Sex differences in COPD management
Published in Expert Review of Clinical Pharmacology, 2021
Maria Gabriella Matera, Josuel Ora, Luigino Calzetta, Paola Rogliani, Mario Cazzola
It has been experimentally shown that dexamethasone is much more active as an anti-inflammatory agent in male than in female mice because of a more potent inhibition of IL-6 and tumor necrosis factor (TNF)-α in male mice [85]. However, always in rodent studies, males were more susceptible to the adverse metabolic effects of chronic corticosteroid exposure [84]. Preclinical studies have documented that receptors for androgens and estrogens can modulate transcriptional regulation by glucocorticoid receptors [84]. Furthermore, both androgens and estrogens can influence the expression and activity of 11β-hydroxysteroid dehydrogenase type 1, an enzyme that enzymatically converts glucocorticoids but does not contribute to the sexually dimorphic effects of synthetic glucocorticoids [84].
Long-term follow-up of a female patient with non-classical 11β-hydroxylase deficiency and two novel mutations in CYP11B1
Published in Gynecological Endocrinology, 2019
Sabina Zacharieva, Ralitsa Robeva, Silvia Andonova, Radoslava Vazharova, Lubomir Balabanski, Maya Atanasoska, Draga Toncheva, Atanaska Elenkova, Alexey Savov
The need of a dexamethasone dose reduction in our patient after the menopause suggested decreased corticosteroid clearance. The metabolic inactivation of dexamethasone has shown interindividual variability and might be influenced by different factors including sex hormone level changes [29,30]. On the other hand, estrogens decrease the 11β-hydroxysteroid dehydrogenase type 1 expression in liver and visceral fat tissues [31]. The 11β-hydroxysteroid dehydrogenases type 1 and type 2 modulate tissue specific balance between the active cortisol and its inert metabolite cortisone [32]. Increased 11β-hydroxysteroid dehydrogenase type 1 activity has been found in postmenopausal compared to premenopausal women suggesting increased local cortisol reactivation [33]. However, the menopause influence on the corticosteroid therapy in patients with CAH remains to be established.