Journal Article
Research Support, Non-U.S. Gov't
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Cellular viability, collagen deposition, and transforming growth factor β1 production among ultraviolet B-irradiated keloid fibroblasts.

BACKGROUND: A keloid is a fibrous tumor produced by fibroblast hyperproliferation and excessive collagen accumulation due to overproduction of transforming growth factor β1 (TGF-β1). High keloid incidence is found among individuals with unexposed skin, especially in Negroid and Mongoloid people with high melanin contents in their skin. Because melanin serves as an ultraviolet B (UVB) light absorber, it is assumed that lack of UVB light penetration may play a role in the keloid pathomechanism. This study aimed to evaluate the effect that UVB irradiation to monolayer keloid fibroblasts has on cell proliferation, collagen deposition, and TGF-β1 production.

METHODS: Keloid fibroblasts were isolated from five patients who underwent surgical treatment. Monolayer cultures of more than three passages of keloid fibroblast were exposed to various dosages of UVB irradiation. Cellular viabilities were measured by MTT assay. Collagen depositions were measured by Sirius Red assay for nonsoluble collagen, and TGF-β1 production was measured by enzyme-linked immunoassay (ELISA). Data were analyzed by one-way analysis of variance (ANOVA).

RESULTS: Ultraviolet B 100 and 150 mJ/cm(2) were able to suppress keloid fibroblast viabilities and collagen accumulation significantly (P < 0.01). Significant suppression of TGF-β1 production required UVB irradiation of 150 mJ/cm(2) (P < 0.01).

CONCLUSIONS: Lack of UVB skin penetration influences the keloid pathomechanism. Ultraviolet B irradiation with a minimal dosage of 150 mJ/cm(2) is a promising method of keloid prevention and treatment.

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