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Updated: Dec 23, 2025

Studying Chronic Exposure of Mice to Ultraviolet B Radiation
Published on: August 19, 2025
Galectin-3 regulates UVB-induced inflammation in skin
Jen-Yu Wang1, Po-Hsuan Lu2, Wan-Wan Lin3
1Department of Dermatology, MacKay Memorial Hospital, Taipei, Taiwan; Mackay Junior College of Medicine, Nursing, and Management, New Taipei City, Taiwan.
Galectin-3 promotes skin inflammation following UVB exposure. Reducing galectin-3 in skin cells and mice lessens UVB-induced damage and inflammatory markers, suggesting a therapeutic target for UV-related skin conditions.
Area of Science:
- Dermatology and immunology research.
- Molecular mechanisms of skin inflammation.
Background:
- Galectin-3 is expressed in skin cells and influences immune responses.
- Its role in ultraviolet (UV) radiation-induced skin inflammation is not well understood.
Purpose of the Study:
- To investigate the role of galectin-3 in human keratinocytes and mouse models of UVB-induced skin inflammation.
Main Methods:
- Used galectin-3 knockdown in human keratinocytes and galectin-3 knockout mice.
- Assessed inflammatory markers (cytokines, proteins, ROS) and skin damage (erythema, TEWL).
Main Results:
- Galectin-3 knockdown reduced UVB-induced inflammation markers like IL-1β and COX2 in keratinocytes.
- Galectin-3 knockout mice exhibited decreased erythema, inflammation, and TEWL after UVB exposure.
Conclusions:
- Galectin-3 plays a significant role in promoting UVB-induced skin inflammation.
- Targeting galectin-3 may offer a strategy for managing UV-related skin damage.
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