The skin is the largest organ of our bodies. It’s the primary interface between our bodies and the environment. The skin function as a barrier to protect our bodies against UV radiation. Epidermis is the outmost layer of our skin and keratinocytes is the major cellular of epidermis.
Subjected to time-of-day dependent changes in the environmental conditions,such as UV radiation. Circadian rhythm are reflected in all cells of the body and meet environmental challenges associated with the solar day. To ensure the proper timing of cellular/metabolic events.
The key elements in maintaining oscillatings at molecular level are Bmal1/Clock, PER/CRY. Bmal1/Clock form a heterodimer, binds to E-box motif in the promoter region of clock controlled genes. Then PER/CRY transcription and form a second heterodimer, prevents the first heterodimer formation and inhibits their own transcription. RORa has a potential ability to bind to the Bmal1 promoter, effectively activate Bmal1 transcription. Participating in circadian rhythm modulated.
Above all, we conclude that uv oscillating Bmal1, Clock, RORa expression and TNFa, IL6, IL8 release in human keratinocytes. Bma1/Clock function as promote apoptosis ans inflammation under UV exposure in human keratinocytes. RORa promote apoptosis and inflammation through Bmal1/Clock under UV exposure in human keratinocytes.This project will provide a new pathway for circadian rhythm modulated by low-dose UVB via changing the expression of clock genes in keratinocytes to prevent aging and carcinogenesis.And low-dose UVB regulates circadian rhythm leading to optimized diagnosis and treatment schedules for skin diseases related to rhythm variation, such as cutaneous pruritus and atopic dermatitis.
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