beta-Carotene interferes with ultraviolet light A-induced gene expression by multiple pathways.

Area of Science:

• Dermatology
• Molecular Biology
• Photobiology

Background:

• Ultraviolet A (UVA) radiation is a primary driver of skin aging.
• Singlet oxygen ((1)O(2)) pathways are implicated in UVA-induced photodamage.
• Beta-carotene (betaC) is a known (1)O(2) quencher.

Purpose of the Study:

• To investigate the effect of beta-carotene pre-treatment on UVA-induced gene regulation in human keratinocytes.
• To elucidate the mechanisms of betaC-UVA interaction in skin cells.
• To determine if betaC's effects are solely mediated by (1)O(2) quenching.

Main Methods:

• Gene expression profiling using microarrays in HaCaT human keratinocytes.
• Assessment of UVA-induced changes in gene expression.
• Analysis of betaC's modulatory effects on UVA-regulated genes.

Main Results:

• UVA exposure altered genes involved in growth factor signaling, inflammation, apoptosis, and cell cycle.
• Beta-carotene modulated the expression of 323 out of 568 UVA-affected genes.
• BetaC inhibited UVA-induced extracellular matrix degradation and enhanced tanning-associated receptor expression.
• BetaC promoted keratinocyte differentiation and synergistically induced cell cycle arrest and apoptosis with UVA exposure.

Conclusions:

• Beta-carotene interacts with UVA effects in keratinocytes through multiple mechanisms, not limited to (1)O(2) quenching.
• Beta-carotene's protective effects are largely independent of its retinoid activity.
• BetaC influences cellular responses to UV radiation, suggesting a role in photoprotection.