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Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
Published on: September 7, 2013
Ultraviolet B(UVB)-induced cox-2 expression in murine skin: an immunohistochemical study
1Department of Dermatology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, New York, 10032, USA.
Biochemical and Biophysical Research Communications
|February 13, 2001
Summary
Chronic UVB exposure increases cyclooxygenase-2 (COX-2) expression in mouse skin, acting as an early marker for sun damage. This elevated COX-2 in skin tumors suggests potential therapeutic benefits of COX-2 inhibitors for preventing skin cancer.
Area of Science:
- Dermatology
- Oncology
- Biochemistry
Background:
- Cyclooxygenase-2 (COX-2) is an enzyme involved in prostaglandin synthesis.
- COX-2 expression is induced by inflammatory agents and mitogens.
- Increased COX-2 expression is observed in various epithelial neoplasms.
Purpose of the Study:
- To investigate the effect of chronic ultraviolet B (UVB) exposure on cutaneous COX-2 expression in mice.
- To assess COX-2 expression in non-tumorigenic skin, benign papillomas, and malignant tumors induced by UVB.
Main Methods:
- SKH-1 mice were subjected to daily UVB irradiation for up to 20 weeks.
- Immunohistochemical analysis was performed to detect COX-2 expression in skin tissues.
- COX-2 expression was evaluated in non-tumor bearing skin, papillomas, and squamous cell carcinomas (SCCs).
Main Results:
- UVB-irradiated mice showed epidermal COX-2 expression, unlike controls.
- COX-2 staining increased progressively with irradiation duration, becoming prominent in the basal cell layer.
- Elevated COX-2 expression was observed in benign papillomas and, more intensely, in well-differentiated SCCs.
Conclusions:
- Cutaneous COX-2 expression serves as an early indicator of UVB exposure.
- COX-2 expression is upregulated during the development of UVB-induced skin tumors.
- Targeting COX-2 with inhibitors may offer a strategy for preventing UVB-induced skin cancer.
