Galectin-3 regulates UVB-induced inflammation in skin
Journal
Journal of Dermatological Science
Journal Volume
98
Journal Issue
2
Pages
119-127
Date Issued
2020
Author(s)
Abstract
Background: Galectin-3 is widely expressed in many immunocytes and epithelial cells including skin keratinocytes. Galectin-3 can regulate immunological or inflammatory processes and plays a proinflammatory role in some disease models. Galectin-3 has a role in disorders related to ultraviolet (UV) photodamage such as apoptosis, skin squamous cell carcinoma and basal cell carcinoma. However, the evidence of galectin-3 in UVB-induced skin inflammation is still limited and the underlying molecular mechanism remains elusive. Objective: We aimed to investigate the effects of galectin-3 in human epidermal keratinocytes and in mice after UVB irradiation. Methods: Primary human epidermal keratinocytes with galectin-3 knockdown were used as the in vitro model. ELISA, QPCR, and western blotting were applied to evaluate the released cytokine, mRNA and protein expression. Histologic analysis, measurement of erythema and transepidermal water loss (TEWL) were applied to evaluate UVB-induced skin damage in galectin-3 knockout mice. Results: In UVB-irradiated human keratinocytes, galectin-3 knockdown downregulated the UVB-induced ASC crosslinking, cleavage of caspase-1, and formation of active IL-1β. Galectin-3 knockdown also decreased UVB-induced production of reactive oxygen species, p38 phosphorylation, and COX2 expression in human keratinocytes. After four days of UVB irradiation, galectin-3 knockout mice showed reduced gross erythema, histologic features of tissue inflammation, quantified levels of erythema and TEWL compared to wild type mice. The skin tissue lysate also showed less expression of active IL-1β and COX2 in galectin-3 knockout mice. Conclusion: Galectin-3 may play a positive regulatory role in UVB-induced skin inflammation. ? 2020
Subjects
Caspase-1; Galectin-3; IL-1β; Inflammasome; Keratinocyte; UV
SDGs
Other Subjects
cyclooxygenase 2; galectin 3; inflammasome; interleukin 1beta; interleukin 1beta converting enzyme; messenger RNA; reactive oxygen metabolite; synaptophysin; cyclooxygenase 2; galectin; galectin 3; interleukin 1beta; interleukin 1beta converting enzyme; LGALS3 protein, human; Lgals3 protein, mouse; plasma protein; reactive oxygen metabolite; adult; animal experiment; animal model; animal tissue; Article; C57BL 6 mouse; controlled study; cross linking; cytokine release; dermatitis; down regulation; enzyme linked immunosorbent assay; erythema; histology; human; human cell; in vitro study; keratinocyte; knockout mouse; male; mouse; nonhuman; polymerase chain reaction; priority journal; protein cleavage; protein expression; protein phosphorylation; skin defect; skin water loss; ultraviolet B radiation; Western blotting; wild type; adverse event; animal; cell culture; cytology; disease model; genetics; immunology; metabolism; pathology; photosensitivity disorder; primary cell culture; radiation response; skin; thermoregulation; ultraviolet radiation; Animals; Blood Proteins; Caspase 1; Cells, Cultured; Cyclooxygenase 2; Disease Models, Animal; Galectin 3; Galectins; Humans; Interleukin-1beta; Keratinocytes; Male; Mice, Knockout; Photosensitivity Disorders; Primary Cell Culture; Reactive Oxygen Species; Skin; Ultraviolet Rays; Water Loss, Insensible
Type
journal article