Glucocorticoid action on skin collagen: overview on clinical significance and consequences

Nuutinen, Pauliina; Autio, Pekka; Hurskainen, Tiina; Oikarinen, Aarne

doi:10.1046/j.0926-9959.2001.00272-4.x

Cited by 15 publications

(15 citation statements)

References 9 publications

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“…Skin atrophy is a well-known and important side effect of GC treatment. GC-induced skin atrophy is reported to be associated with decreased expression of collagen type I and type III [3], [4], [34]. However, all these reports analyzed the effects of a pharmacological dose of GC on skin collagen metabolism.…”

Section: Discussionmentioning

confidence: 99%

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11β-Hydroxysteroid Dehydrogenase 1 Specific Inhibitor Increased Dermal Collagen Content and Promotes Fibroblast Proliferation

et al. 2014

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Glucocorticoids (GCs) are one of the most effective anti-inflammatory drugs for treating acute and chronic inflammatory diseases. However, several studies have shown that GCs alter collagen metabolism in the skin and induce skin atrophy. Cortisol is the endogenous GC that is released in response to various stressors. Over the last decade, extraadrenal cortisol production in various tissues has been reported. Skin also synthesizes cortisol through a de novo pathway and through an activating enzyme. 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) is the enzyme that catalyzes the conversion of hormonally inactive cortisone to active cortisol in cells. We previously found that 11β-HSD1 negatively regulates proliferation of keratinocytes. To determine the function of 11β-HSD1 in dermal fibroblasts and collagen metabolism, the effect of a selective 11β-HSD1 inhibitor was studied in mouse tissues and dermal fibroblasts. The expression of 11β-HSD1 increased with age in mouse skin. Subcutaneous injection of a selective 11β-HSD1 inhibitor increased dermal thickness and collagen content in the mouse skin. In vitro, proliferation of dermal fibroblasts derived from 11β-HSD1 null mice (Hsd11b1−/− mice) was significantly increased compared with fibroblasts from wild-type mice. However, in vivo, dermal thickness of Hsd11b1−/− mice was not altered in 3-month-old and 1-year-old mouse skin compared with wild-type mouse skin. These in vivo findings suggest the presence of compensatory mechanisms in Hsd11b1−/− mice. Our findings suggest that 11β-HSD1 inhibition may reverse the decreased collagen content observed in intrinsically and extrinsically aged skin and in skin atrophy that is induced by GC treatment.

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Section: Discussionmentioning

confidence: 99%

“…Skin atrophy is a known side effect of both topical and systemic GC treatment[1], [2]. Several studies show that GCs alter collagen metabolism in the skin [3], [4], [5].…”

Section: Introductionmentioning

confidence: 99%

11β-Hydroxysteroid Dehydrogenase 1 Specific Inhibitor Increased Dermal Collagen Content and Promotes Fibroblast Proliferation

et al. 2014

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“…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). This results in a reorganization of the collagen fibers in which dense, compact bundles are formed in place of the more structurally sound “basketweave” meshwork (12).…”

Section: Introductionmentioning

confidence: 96%

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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“…The clinically best‐known side‐effects include atrophy of the skin and osteoporosis, which are mainly due to altered collagen metabolism. During recent years, the biochemical mechanisms of these side‐effects have become better understood, largely due to new methods of studying collagen metabolism in vivo 2 …”

mentioning

confidence: 99%

“…It has been shown that systemic, topical and even inhaled glucocorticoids decrease collagen synthesis in the skin when used for a long time 2–7 . This decrease is one of the main events leading to skin atrophy.…”

mentioning

confidence: 99%

Modulation of collagen synthesis and mRNA by continuous and intermittent use of topical hydrocortisone in human skin

et al. 2003

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Glucocorticoid action on skin collagen: overview on clinical significance and consequences

Cited by 15 publications

References 9 publications

11β-Hydroxysteroid Dehydrogenase 1 Specific Inhibitor Increased Dermal Collagen Content and Promotes Fibroblast Proliferation

11β-Hydroxysteroid Dehydrogenase 1 Specific Inhibitor Increased Dermal Collagen Content and Promotes Fibroblast Proliferation

Longitudinal in vivo tracking of adverse effects following topical steroid treatment

Modulation of collagen synthesis and mRNA by continuous and intermittent use of topical hydrocortisone in human skin

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