In Vivo Prevention of Corticosteroid-Induced Skin Atrophy by Tretinoin in the Hairless Mouse Is Accompanied by Modulation of Collagen, Glycosaminoglycans, and Fibronectin

Schwartz, Ernest; Mezick, James A.; Gendimenico, Gerard J.; Kligman, Lorraine H.

doi:10.1111/1523-1747.ep12371770

Cited by 38 publications

(29 citation statements)

References 51 publications

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“…The reduction of adrenal hyperplasia could be due to the reduction in ACTH levels as well as to the direct inhibition of adrenal cell proliferation. The reversion of skin atrophy is in line with previous studies that show that retinoic acid can reverse the changes produced by glucocorticoids on dermal connective tissue (41). Therefore, retinoic acid could reverse the symptoms in the skin by a direct mechanism that may concur with the hormonal inhibition and the antitumorigenic effects.…”

Section: Discussionsupporting

confidence: 89%

Retinoic acid prevents experimental Cushing syndrome

Páez-Pereda¹,

Kovalovsky²,

Hopfner³

et al. 2001

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 89%

Retinoic acid prevents experimental Cushing syndrome

Páez-Pereda¹,

Kovalovsky²,

Hopfner³

et al. 2001

J. Clin. Invest.

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“…TOXICOLOGIC PATHOLOGY surrounding lamina propria of all corticosteroid treated groups compared with concurrent controls. This positive effect of corticosteroid on fibroblast fibronectin production has been reported previously in the skin of the hairless mouse (Schwartz et al 1994). Masson's trichrome stained the lamina propria uniformly blue in treated animals, indicating the presence of Corticosterone data not reported at 36 weeks or recovery due to analytical difficulties.…”

Section: Discussionsupporting

confidence: 85%

Hyalinization of the Pyloric Stomach in CD-1 Mice Following Oral (Dietary) Administration of the Corticosteroid Agonists Mometasone Furoate, Budesonide, and Flunisolide

et al. 2011

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The purpose of this study was to compare the toxicity of three marketed corticosteroid receptor agonists (mometasone furoate, budesonide, or flunisolide) to the stomach of female CD-1 mice following oral administration via the diet for up to 52 weeks, with a 16-week recovery period (budesonide and flunisolide). A range of tissues was examined by light microscopy, accompanied by clinical pathology measurements to assess anticipated corticosteroid effects as a surrogate marker of systemic drug exposure. Microscopic changes seen in the stomach with each corticosteroid included pyloric hyalinization. This previously unreported finding was investigated using histochemical and immunohistochemical techniques and was found to consist of hyalinized collagen, in association with increased immunohistochemical signal for transglutaminase-2 and osteopontin. The significance of the osteopontin finding is unclear; however, the ability of transglutaminase-2 to facilitate the formation of degradation resistant protein bonds implies this protein may be involved in the pathogenesis of this change. Furthermore, published evidence that transglutaminase-2 may be induced by a corticosteroid agonist raises the possibility that pyloric stomach hyalinization may be a class effect of corticosteroids via the action of this enzyme.

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“…33,42 On the molecular level, various proteins like glucosaminoglycan, fibronectin and collagens may be used as indicators of GC effects. 39,43 Beside the direct parameters of skin atrophy, systemic effects of topically administered compounds can also be measured such as weight loss of body, thymus, spleen and adrenal glands. 34,35,39 The pros of in vivo pre-clinical tests compared to clinical tests are the reduced variability, higher cost-efficiency and in particular ethical aspects ( Table 1).…”

Section: 34mentioning

confidence: 99%