1136 Galectin-3 regulates UVB-induced inflammation in skin

Abstract

Galectin-3, a β-galactoside binding lectin, can be detected in diverse types of cells, including epidermal keratinocytes. Regulatory roles of galectin-3 in the pathogenesis of various malignant and inflammatory skin disorders have been reported, but the known roles of galectin-3 in UVB-induced inflammation in skin are still limited and the underlying molecular mechanisms remain elusive. In this study, we aimed to evaluate the regulatory roles of galectin-3 in UVB-induced inflammatory responses in skin by using primary normal human epidermal keratinocytes (NHEKs) and galectin-3 knockout mice as the models. Our results demonstrated knockdown of galectin-3 in NHEKs attenuated the UVB-induced production of active IL-. UVB-induced ASC cross-linking and active caspase-1 formation were reduced but LDH release was not affected after galectin-3 knockdown. In addition, after galectin-3 knockdown, UVB-induced IL-8, TNF-α and COX-2 expression in NHEKs were also down-regulated. Furthermore, UVB-induced production of reactive oxygen species in NHEKs was also reduced after galectin-3 knockdown. In the animal study, UVB-induced skin inflammation and damage were less severe in galectin-3 knockout mice than in wild type mice grossly and histologically. When measuring the physiological parameters, UVB-induced transepidermal water loss and skin erythema index were also reduced in galectin-3 knockout mice compared with wild type mice. In conclusion, current findings indicate that galectin-3 plays a crucial regulatory role in UVB-induced inflammation, suggesting a potential way to prevent UVB-induced skin damage by targeting galectin-3 in skin.