β-Carotene Interferes with Ultraviolet Light A-Induced Gene Expression by Multiple Pathways

Abstract

Ultraviolet light A (UVA) exposure is thought to cause skin aging mainly by singlet oxygen ((1)O(2))-dependent pathways. Using microarrays, we assessed whether pre-treatment with the (1)O(2) quencher beta-carotene (betaC; 1.5 microM) prevents UVA-induced gene regulation in HaCaT human keratinocytes. Downregulation of growth factor signaling, moderate induction of proinflammatory genes, upregulation of immediate early genes including apoptotic regulators and suppression of cell cycle genes were hallmarks of the UVA effect. Of the 568 UVA-regulated genes, betaC reduced the UVA effect for 143, enhanced it for 180, and did not interact with UVA for 245 genes. The different interaction modes imply that betaC/UVA interaction involved multiple mechanisms. In unirradiated keratinocytes, gene regulations suggest that betaC reduced stress signals and extracellular matrix (ECM) degradation, and promoted keratinocyte differentiation. In irradiated cells, expression profiles indicate that betaC inhibited UVA-induced ECM degradation, and enhanced UVA induction of tanning-associated protease-activated receptor 2. Combination of betaC-promoted keratinocyte differentiation with the cellular "UV response" caused synergistic induction of cell cycle arrest and apoptosis. In conclusion, betaC at physiological concentrations interacted with UVA effects in keratinocytes by mechanisms that included, but were not restricted to (1)O(2) quenching. The retinoid effect of betaC was minor, indicating that the betaC effects reported here were predominantly mediated through vitamin A-independent pathways.

Photoprotective compounds from marine organisms

“…It has been shown that b-carotene can modulate UV-A-induced gene expression in human keratinocytes [221]. Carotenoids have also been assessed in relation with their antioxidant properties [47] that can play a key role in reducing the incidence of several UVR-mediated diseases [6].…”

Influence of Topical, Systemic and Combined Application of Antioxidants on the Barrier Properties of the Human Skin

“…This, in turn, leads to degradation, e.g. of the extracellular matrix proteins, by inducing matrix metalloproteases [30]. On the contrary, antioxidants such as β-carotene significantly reduce stress and degradation of the extracellular matrix, in addition to promoting the differentiation of keratinocytes [31], which might explain the improved skin parameters that we observed.…”

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“…There are quite a few natural compounds, which can prevent from UV damage: α-tocopherol which prevents UVA-and UVB-induced glutathione loss and reduce induction of DNA damage by UVB [19,20]. β-Carotene which inhibits free radicals and cause higher resistance to immunosuppression after exposure to UV light [21]; lycopene which absorb light in the UV range and increase the toughness of the skin [22,23]. Lutein which prevent extracellular matrix breakdown and prevents skin from UV damage [24]; flavonoids such as isorhamnetin, quercetin, kaempferol which significantly decreased erythema developed after UVB irradiation [25], and green tea polyphenols which reduce UV-induced p53 expression and keratinocytes apoptosis and protect from DNA damage [26], and others.…”