Microvascular effects of corticotropin-releasing hormone in human skin vary in relation to estrogen concentration during the menstrual cycle

Clifton, Vicki L.; Crompton, Renee; Read, Mark; Gibson, Peter G.; Smith, Roger; Wright, Ian

doi:10.1677/joe.1.06030

Cited by 15 publications

(10 citation statements)

References 60 publications

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“…However, at the microcirculatory level, it has been recently shown that the menstrual cycle had no effect on skin endothelial vasodilation tested with ACh iontophoresis (9). In our study, there is no statistical difference in the phase of the cycle between BDC-7 and HDT ϩ 56.…”

Section: Discussioncontrasting

confidence: 66%

WISE 2005: chronic bed rest impairs microcirculatory endothelium in women

Demiot¹,

Dignat-George²,

Fortrat³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Sedentary behavior has deleterious effects on the cardiovascular system, including reduced endothelial functions. A 2-mo bed rest study in healthy women [women international space simulation for exploration (WISE) 2005 program] presented a unique opportunity to analyze the specific effects of prolonged inactivity without other vascular risk factors on the endothelium. We investigated endothelial properties before and after 56 days of bed rest in 8 subjects who performed no exercise (control group: No-EX) and in 8 subjects who regularly performed treadmill exercise in a lower body negative pressure chamber as well as resistance exercise (countermeasure group, EX). A functional evaluation of the microcirculation in the skin was assessed with laser Doppler. We studied endothelium-dependent and -independent vasodilation using iontophoresis of acetylcholine and sodium nitroprusside, respectively. We also measured circulating endothelial cells (CECs), an index of endothelial damage. In the No-EX group, endothelium-dependent vasodilation was significantly reduced (35.4 +/- 4.8% vs. 24.1 +/- 3.8%, P < 0.05) by bed rest with a significant increase in the number of CECs (3.6 +/- 1.4 vs. 10.6 +/- 2.7 ml(-1), P < 0.05). In the EX group, endothelium-dependent vasodilation and number of CECs were preserved. Our study shows that in humans prolonged bed rest causes impairment of endothelium-dependent function at the microcirculatory level, along with an increase in circulating endothelial cells. Microcirculatory endothelial dysfunction might participate in cardiovascular deconditioning, as well as in several bed rest-induced pathologies. We therefore conclude that the endothelium should be a target for countermeasures during periods of prolonged deconditioning.

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Section: Discussioncontrasting

confidence: 66%

WISE 2005: chronic bed rest impairs microcirculatory endothelium in women

Demiot¹,

Dignat-George²,

Fortrat³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, findings on the impact of hormone levels such as serum oestradiol on PORH in microcirculation are inconsistent [45,46]. Regarding the proportion of female study participants in both groups, a subgroup analysis addressing the stages of the menstrual cycle would have considerably lowered the statistical power of our study.…”

Section: Discussionmentioning

confidence: 88%

Microvascular autoregulation in children and adolescents with type 1 diabetes mellitus

et al. 2012

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Aims/hypothesis Deterioration of microvascular function may have an early onset in individuals with type 1 diabetes mellitus. We hypothesised that microvascular autoregulation is impaired in children with type 1 diabetes and can be detected non-invasively by postocclusive reactive hyperaemia (PORH). Methods Microvascular autoregulation was assessed in 58 children with type 1 diabetes and 58 age-and sex-matched healthy controls by PORH using laser Doppler fluxmetry. Baseline perfusion, biological zero (defined as a 'no flow' laser Doppler signal during suprasystolic occlusion), peak perfusion following occlusion, time to peak and recovery time (time until baseline perfusion is resumed) were recorded and compared between the groups.Results Peak perfusion was higher in children with type 1 diabetes than in healthy controls (1.7±0.93 AU [arbitrary units] vs 1.29±0.46 AU; p00.004), and biological zero was lower in children with type 1 diabetes vs controls (0.14± 0.04 AU vs 0.19±0.04 AU; p<0.0001). No differences were seen between the groups in baseline perfusion, time to peak during PORH and recovery time following PORH. Conclusions/interpretation PORH reveals impaired microvascular autoregulation in children with type 1 diabetes. The higher peak perfusion might reflect a decline in the vasoconstrictive ability of arteriolar smooth muscle cells upstream of capillary beds in children with type 1 diabetes.

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“…CRH can also modify DNA synthesis in the dermal and epidermal compartments of cultured mouse skin depending on the phase of the hair growth cycle (24). These differential effects are apparently related to fluctuations in CRH-R1 and CRH-R2 expression during the hair growth cycle (20,24,65) Skin vasculature is a recognized target for CRH and urocortin peptides (6,(77)(78)(79), where, depending on the animal model used, CRH can induce local vascular dilatation (6,(77)(78)(79) and either inhibit or stimulate angiogenesis (80,81). Interestingly, both CRH and urocortin demonstrated anti-edema effects (82)(83)(84).…”

Section: Phenotypic Effects Of Crh and Urocortin In Cultured Skin Cellsmentioning

confidence: 99%

“…In the specific case of human skin, Clifton et al clearly have shown vasodilatory action of CRH, mediated by mechanisms that included both indirect effects, activation of mast cells or endothelial-dependent pathways, and a direct action on the blood vessel wall (77)(78)(79). These vascular effects of CRH appear to be dependent on the local level of estrogenization (77).…”

Section: Phenotypic Effects Of Crh and Urocortin In Cultured Skin Cellsmentioning

confidence: 99%

Corticotropin releasing hormone and the skin

Słomiński¹

2006

Front Biosci

139

228

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Cotricotropin-releasing hormone (CRH) and related peptides are produced in skin that is dependent on species and anatomical location. Local peptide production is regulated by ultraviolet radiation (UVR), glucocorticoids and phase of the hair cycle. The skin also expresses the corresponding receptors (CRH-R1 and CRH-R2), with CRH-R1 being the major receptor in humans. CRH-R1 is expressed in epidermal and dermal compartments, and CRH-R2 predominantly in dermal structures. The gene coding for CRH-R1 generates multiple isoforms through a process modulated by UVR, cyclic adenosine monophosphate (cAMP) and phorbol 12-myristate 13-acetate. The phenotypic effects of CRH in human skin cells are largely mediated by CRH-R1alpha through increases in concentrations of cAMP, inositol triphosphate (IP 3 ), or Ca 2+ with subsequent activation of protein kinases A (PKA) and C (PKC) dependent pathways. CRH also modulates the activity of nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-kappaB), activator protein 1 (AP-1) and cAMP responsive element binding protein (CREB). The cellular functions affected by CRH depend on cell type and nutritional status and include modulation of differentiation program(s), proliferation, viability and immune activity. The accumulated evidence indicates that cutaneous CRH is also a component of a local structure organized similarly to the hypothalamo-pituitary-adrenal axis. KeywordsHuman Skin; Hormone; Corticotropin; CRH; CRH-R1; CRH-R2; Urocortin; Review INTRODUCTIONCRH is the central trigger of HPA axis, and together with related peptides urocortin I-III also regulate behavioral, autonomic, endocrine, reproductive, cardiovascular, gastro-intestinal, metabolic and immune systemic functions (1-11). Other actions include local immunomodulatory (predominantly proinflammatory) effects (12)(13)(14), differing from a central immunosuppressive activity (through the HPA axis) (3). Of note, locally produced CRH can directly regulate steroid hormone production by adrenals and gonads (1,2). Furthermore, CRH in the immune cells can induce production and release of proopiomelanocortin (POMC) derived adrenocorticotropin (ACTH) and beta-endorphin peptides. NIH Public Access Author ManuscriptFront Biosci. Author manuscript; available in PMC 2007 April 2. Published in final edited form as:Front Biosci. ; 11: 2230-2248. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptIn vertebrates these peptides interact with membrane-bound CRH-R1 and CRH-R2 (1,2). Both receptor types belong to the group II subfamily of G protein-coupled receptors (GPCRs). CRH-R1 binds CRH and urocortin I with high affinity; it does not bind urocortin II (strescopin related protein). CRH-R2 shows preferential affinity for urocortin II, although it also binds CRH, however, with lower affinity than CRH-R1. Signal transduction through CRH-Rs is coupled to the activation of adenylate cyclase (AC), phospholipase C (PLC) and calcium channels (1, 2,5,6). ALTERNATIVELY SPLICED CRH-RS ISOFORMS: AN OVER...

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Microvascular effects of corticotropin-releasing hormone in human skin vary in relation to estrogen concentration during the menstrual cycle

Cited by 15 publications

References 60 publications

WISE 2005: chronic bed rest impairs microcirculatory endothelium in women

WISE 2005: chronic bed rest impairs microcirculatory endothelium in women

Microvascular autoregulation in children and adolescents with type 1 diabetes mellitus

Corticotropin releasing hormone and the skin

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