PARP-1 ACTIVITY IS INVOLVED IN THE SOLAR UV-INDUCED CUTANEOUS INFLAMMATORY RESPONSE IN THE EPIDERM-FT IN VITRO HUMAN SKIN MODEL.
Poly (ADP-ribose) polymerase 1 (PARP-1) is known to be activated under conditions of genotoxic stress. In the presence of DNA damage, PARP-1, a nuclear zinc-finger DNA-binding protein, is activated and catalyzes the transfer of ADP-ribose from NAD+ to itself (automodification) and a range of other nuclear proteins (1,2,3). UV-induced cutaneous inflammation has been demonstrated in several models and appears to occur through the activation of Nuclear Factor kappa B (NF-кB) (4,5). In the present study, the EpiDerm-FT in vitro human skin model (EFT-400) was used to gain insight into the mechanisms of the UV-induced inflammatory response of human epidermal tissue. The EpiDerm-FT model consists of a 3-demensional, highly differentiated epidermis cultured with normal human epidermal keratinocytes cultured on a collagen dermis populated with normal human dermal fibroblasts. The model exhibits stratified epidermal components and a fully developed basement membrane at the dermal/epidermal junction.
Apoptotic sunburn cells, CCL11, CCL21, CCL26, CCL3, CCL4, CSF2, CXCL10, Cyclopyrimidine dimer assay , EFT-400, EpiDerm, G-CSF, GM-CSF, IL18, IL1B, IL-1α, IL6, IL-6, IL8, IL-8, ILJA, Inflammatory genes, IP-10, Nuclear factor kappa B, Nuclear zinc-finger DNA binding protein, Poly (ADP-ribose) polymerase 1 (PARP-1), RANTES, Sunburn cells, UV exposure
4 amino-1,8-napthalamide, UVA, UVB
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