Glucocorticoids and the Cardiovascular System

Goodwin, Julie E.

doi:10.1007/978-1-4939-2895-8_13

Cited by 16 publications

(12 citation statements)

References 89 publications

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“…Hypercortisolism, whether in the form of endogenous Cushing's syndrome or induced by therapeutic glucocorticoid administration, affects skin physiology in a variety of ways (Sevilla and Pé rez, 2018;Stratakis, 2016). In addition, glucocorticoids have been hypothesized to induce hypertension by direct interaction with vascular smooth muscle cells, inducing vasoconstriction (Goodwin, 2015). Because skin and vascular function are major factors in mouse insulation, we investigated to which extent CORT affects the animal's heat retention capacity and thereby influences the environmental temperature range over which the animal must expend the least amount of energy to defend its body temperature (i.e., the thermoneutral zone).…”

Section: Long-term Corticosterone Treatment Leads To a Progressive Inmentioning

confidence: 99%

Glucocorticoid-Induced Obesity Develops Independently of UCP1

et al. 2019

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Section: Long-term Corticosterone Treatment Leads To a Progressive Inmentioning

confidence: 99%

Glucocorticoid-Induced Obesity Develops Independently of UCP1

et al. 2019

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“…Bone fragility is significantly increased during treatment with glucocorticoids, powerful drugs used in anti-inflammatory and immunosuppressive therapy, for instance to treat asthma, rheumatoid arthritis, or inflammatory bowel disease (4, 5). Despite their unmistakable advantages, therapeutic treatment with glucocorticoids causes metabolic alterations which can lead to insulin resistance, and other problems, e.g., high blood pressure (6, 7). Treatment induced bone fragility partly results from direct effects of excess glucocorticoids on bone forming osteoblasts, which show reduced proliferation (8, 9).…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid Treatment Leads to Aberrant Ion and Macromolecular Transport in Regenerating Zebrafish Fins

et al. 2019

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Long-term glucocorticoid administration in patients undergoing immunosuppressive and anti-inflammatory treatment is accompanied by impaired bone formation and increased fracture risk. Furthermore, glucocorticoid treatment can lead to impaired wound healing and altered cell metabolism. Recently, we showed that exposure of zebrafish to the glucocorticoid prednisolone during fin regeneration impacts negatively on the length, bone formation, and osteoblast function of the regenerate. The underlying cellular and molecular mechanisms of impairment, however, remain incompletely understood. In order to further elucidate the anti-regenerative effects of continued glucocorticoid exposure on fin tissues, we performed proteome profiling of fin regenerates undergoing prednisolone treatment, in addition to profiling of homeostatic fin tissue and fins undergoing undisturbed regeneration. By using LC-MS (liquid chromatography-mass spectrometry) we identified more than 6,000 proteins across all tissue samples. In agreement with previous reports, fin amputation induces changes in chromatin structure and extracellular matrix (ECM) composition within the tissue. Notably, prednisolone treatment leads to impaired expression of selected ECM components in the fin regenerate. Moreover, the function of ion transporting ATPases and other proteins involved in macromolecule and vesicular transport mechanisms of the cell appears to be altered by prednisolone treatment. In particular, acidification of membrane-enclosed organelles such as lysosomes is inhibited. Taken together, our data indicate that continued synthetic glucocorticoid exposure in zebrafish deteriorates cellular trafficking processes in the regenerating fin, which interferes with appropriate tissue restoration upon injury.

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“…The presence of ED is recognized as the Primum movens of atherogenesis, and as such is a seminal target for reducing CV risk in RA [3]. In addition, GCs may modulate vascular function directly, as GC receptors are expressed by both endothelial and vascular smooth muscle cells (VSMC) [7]. Despite a significant evolution in the treatment of RA, the majority of patients still use GCs alone or in combination with diseasemodifying anti-rheumatic drugs (DMARDs).…”

Section: Introductionmentioning

confidence: 99%

“…However, GCs might also decrease CV risk by decreasing the systemic and/or vascular inflammation. In addition, GCs may modulate vascular function directly, as GC receptors are expressed by both endothelial and vascular smooth muscle cells (VSMC) [7]. Recent reviews addressing the effects of GCs on CV risk in RA yielded conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids improve endothelial function in rheumatoid arthritis: a study in rats with adjuvant-induced arthritis

Verhoeven

Totoson

Maguin‐Gaté

et al. 2017

Clinical and Experimental Immunology

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To determine the effect of glucocorticoids (GCs) on endothelial dysfunction (ED) and on traditional cardiovascular (CV) risk factors in the adjuvant-induced arthritis (AIA) rat model. At the first signs of AIA, a high dose (HD) [10 mg/kg/day, intraperitoneally (i.p.), GC-HD] or low dose (LD) (1 mg/kg/day, i.p., GC-LD) of prednisolone was administered for 3 weeks. Endothelial function was studied in aortic rings relaxed with acetylcholine (Ach) with or without inhibitors of nitric oxide synthase (NOS), cyclooxygenase 2 (COX-2), arginase, endothelium derived hyperpolarizing factor (EDHF) and superoxide anions ( O2-°) production. Aortic expression of endothelial NOS (eNOS), Ser1177-phospho-eNOS, COX-2, arginase-2, p22 and p47 was evaluated by Western blotting analysis. Arthritis scores, blood pressure, heart rate and blood levels of cytokines, triglycerides, cholesterol and glucose were measured. GC-HD but not GC-LD reduced arthritis score significantly and improved Ach-induced relaxation (P < 0·05). The positive effect of GC-HD resulted from increased NOS activity and EDHF production and decreased COX-2/arginase activities and O2-° production. These functional effects relied upon increased phospho-eNOS expression and decreased COX-2, arginase-2 and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression. Despite the lack of effect of GC-LD on ED, it increased NOS and EDHF and down-regulated O2-° pathways but did not change arginase and COX-2 pathways. GC-HD increased triglycerides levels and blood pressure significantly (P < 0·05). Both doses of GCs decreased to the same extent as plasma interleukin (IL)-1β and tumour necrosis factor (TNF)-α levels (P < 0·05). Our data demonstrated that subchronic treatment with prednisolone improved endothelial function in AIA via pleiotropic effects on endothelial pathways. These effects occurred independently of the deleterious cardiometabolic effects and the impact of prednisolone on systemic inflammation.

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Glucocorticoids and the Cardiovascular System

Cited by 16 publications

References 89 publications

Glucocorticoid-Induced Obesity Develops Independently of UCP1

Glucocorticoid-Induced Obesity Develops Independently of UCP1

Glucocorticoid Treatment Leads to Aberrant Ion and Macromolecular Transport in Regenerating Zebrafish Fins

Glucocorticoids improve endothelial function in rheumatoid arthritis: a study in rats with adjuvant-induced arthritis

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