Selective Action Of Hydrocortisone On Postmitotic Epidermal Cells In Vivo

Laurence, Edna B.; Christophers, Enno

doi:10.1111/1523-1747.ep12482145

Cited by 42 publications

(19 citation statements)

References 8 publications

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“…Prior work has shown that long-term GC treatment decreases epidermal proliferation and differentiation (Laurence and Christophers, 1976;du Vivier et al, 1982;Sheu et al, 1991;Sheu et al, 1997). But even short-term GC treatment inhibits epidermal lipid synthesis, resulting in decreased production and secretion of lamellar bodies (LB), and impaired production of lamellar membranes in the SC (Kao et al, 2003).…”

mentioning

confidence: 99%

Mechanisms by Which Psychologic Stress Alters Cutaneous Permeability Barrier Homeostasis and Stratum Corneum Integrity

Choi

Brown

Crumrine

et al. 2005

Journal of Investigative Dermatology

179

144

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Although many skin disorders, including psoriasis and atopic dermatitis, are adversely affected by psychologic stress (PS), the pathophysiologic link between PS and disease expression remains unclear. Recent studies demonstrated PS-induced alterations in permeability barrier homeostasis, mediated by increased endogenous glucocorticoids. Here, we assessed the mechanisms by which PS alters stratum corneum (SC) function. Insomniac psychologic stress (IPS) altered both barrier homeostasis and SC integrity. IPS decreased epidermal cell proliferation, impaired epidermal differentiation, and decreased the density and size of corneodesmosomes (CD), which was linked to degradation of CD proteins (e.g., desmoglein1). Barrier compromise was linked to decreased production and secretion of lamellar bodies (LB), which in turn could be attributed to a decrease in de novo synthesis of epidermal lipids. Topical physiologic lipids (equimolar cholesterol, ceramides, and free fatty acids) normalized both barrier homeostasis and SC integrity in IPS mice, further evidence that lipid deficiency accounted for these functional abnormalities. Thus, PS inhibition of epidermal lipid synthesis results in decreased LB formation and secretion, as well as decreased CD, compromising both permeability barrier homeostasis and SC integrity. These studies suggest that topical treatment with epidermal physiologic lipids could be beneficial in stress-induced, barrier-associated dermatoses, such as psoriasis and atopic dermatitis.

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mentioning

confidence: 99%

Mechanisms by Which Psychologic Stress Alters Cutaneous Permeability Barrier Homeostasis and Stratum Corneum Integrity

Choi

Brown

Crumrine

et al. 2005

Journal of Investigative Dermatology

179

144

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“…As well as the rate of DNA synthesis chalones affect the transit rate through the Gj phase (G! inhibitor) and the mitotic rate (G2 inhibitor) of the cell cycle [Iversen, 1969;Hennings et al, 1969;Elgjo et al, 1971Elgjo et al, , 1972Houck and Daugherty, 1974;Elgjo, 1974], Adrenaline is regarded to amplify the chalone activity [Bullough and Rytomaa, 1965], but adrenaline itself as well as cortisol have little, if any, antimitotic effects Laurence, 1964, 1968;Laurence and Christophers, 1976].…”

mentioning

confidence: 99%

Human Epidermal Cell Proliferation with Regard to Circadian Variation of Plasma Cortisol

Schell¹,

Hornstein²,

Schwarz³

1980

Dermatology

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This study was performed in 6 healthy young men under analogous experimental conditions to investigate whether or not the epidermal proliferative activity is influenced by the physiological circadian rhythmicity of cortisol concentration in blood. Every 6 h of total duration of the experiments, blood samples were taken for radioimmunoassay of serum cortisol and skin punch biopsies (upper arm inside) were labelled in vitro by ³H-thymidine. In 4 out of 6 individuals, an inverse and time-shifted correlation between the combined serum cortisol levels and the epidermal ³H-LI could be found, i.e., a rise or decline of serum cortisol were followed by a lowered or elevated rate of epidermal LI 6 h later. In particular, a steep increase of serum cortisol from midnight to 6 a.m. correlated to a decrease of ³H-LI from 6 a.m. to noon. This indicates that in man the rate of the epidermal proliferative activity inversely depends, apart from other mechanisms of regulation, on the concentration and circadian periodicity of endogenous cortisol in blood. However, we failed to demonstrate a clear circadian rhythm of the epidermal proliferation, possibly due to the short duration of the experiments extended in each individual to 48 h only.

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“…Epidermal atrophy and thinning due to topical corticosteroid treatment has been characterized previously, and increased rates of cell differentiation without a corresponding increase in cell proliferation rates were identified (10). Thus, keratinocytes were observed to mature at faster rates, differentiating to corneocytes and ultimately being shed off before basal cells are able to divide and replace these lost cells.…”

Section: Discussionmentioning

confidence: 93%

“…Topical steroids have also been shown to decrease the proliferation rates of keratinocytes and fibroblasts (8, 9) as well as accelerate the maturation of these cells (10). A decrease in Type I collagen production by dermal fibroblasts has also been observed (11).…”

Section: Introductionmentioning

confidence: 99%

Longitudinal in vivo tracking of adverse effects following topical steroid treatment

Bower

Arp

Zhao

et al. 2016

Experimental Dermatology

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Topical steroids are known for their anti-inflammatory properties and are commonly prescribed to treat many adverse skin conditions such as eczema and psoriasis. While these treatments are known to be effective, adverse effects including skin atrophy are common. In this study, the progression of these effects is investigated in an in vivo mouse model using multimodal optical microscopy. Utilizing a system capable of performing two-photon excitation fluorescence microscopy (TPEF) of reduced nicotinamide adenine dinucleotide (NADH) to visualize the epidermal cell layers and second harmonic generation (SHG) microscopy to identify collagen in the dermis, these processes can be studied at the cellular level. Fluorescence lifetime imaging microscopy (FLIM) is also utilized to image intracellular NADH levels to obtain molecular information regarding metabolic activity following steroid treatment. In this study, fluticasone propionate (FP) treated, mometasone furoate (MF) treated, and untreated animals were imaged longitudinally using a custom-built multimodal optical microscope. Prolonged steroid treatment over the course of 21 days is shown to result in a significant increase in mean fluorescence lifetime of NADH, suggesting a faster rate of maturation of epidermal keratinocytes. Alterations to collagen organization and the structural microenvironment are also observed. These results give insight into the structural and biochemical processes of skin atrophy associated with prolonged steroid treatment.

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Selective Action Of Hydrocortisone On Postmitotic Epidermal Cells In Vivo

Cited by 42 publications

References 8 publications

Mechanisms by Which Psychologic Stress Alters Cutaneous Permeability Barrier Homeostasis and Stratum Corneum Integrity

Mechanisms by Which Psychologic Stress Alters Cutaneous Permeability Barrier Homeostasis and Stratum Corneum Integrity

Human Epidermal Cell Proliferation with Regard to Circadian Variation of Plasma Cortisol

Longitudinal in vivo tracking of adverse effects following topical steroid treatment

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