TY - JOUR
T1 - Role of PKC isozymes in low power light - Stimulated proliferation of cultured skin cells
AU - Grossman, Nili
AU - Kleitman, Vered
AU - Meller, Julia
AU - Kaufmann, Roland
AU - Akgun, Nermin
AU - Ruck, Angelika
AU - Livneh, Etta
AU - Lubart, Rachel
PY - 2000
Y1 - 2000
N2 - Exposure of cultured skin cells to low power visible light leads to a transiently stimulated proliferation. Facilitation of this response requires the presence of active PKC, elevation of intracellular calcium, and involves reactive oxygen species. In the present study, the role of PKCα and PKCν was examined using paired murine fibroblasts, differing in the level of these isozymes expression. The ability of the cells to respond to low power UVA light or HeNe laser by stimulated proliferation was correlated with an activated state or overexpression of PKCα, but not PKCν. A parallel response was obtained in cells that were loaded with AlPcS4 before photosensitization. Whenever this latter treatment caused a light-stimulated inhibition, it was accompanied by the intracellular calcium and photosensitizer dynamics typical of the effect of PDT on rat epithelial cells. Accordingly, added antioxidants that suppressed light-stimulated proliferation also suppressed this light-stimulated inhibition. The model systems employed in this study are the first to demonstrate the specific effect of PKC isozymes on light-stimulated proliferation, in relation to oxidative stress, and indicate their dual role in light-tissue interaction.
AB - Exposure of cultured skin cells to low power visible light leads to a transiently stimulated proliferation. Facilitation of this response requires the presence of active PKC, elevation of intracellular calcium, and involves reactive oxygen species. In the present study, the role of PKCα and PKCν was examined using paired murine fibroblasts, differing in the level of these isozymes expression. The ability of the cells to respond to low power UVA light or HeNe laser by stimulated proliferation was correlated with an activated state or overexpression of PKCα, but not PKCν. A parallel response was obtained in cells that were loaded with AlPcS4 before photosensitization. Whenever this latter treatment caused a light-stimulated inhibition, it was accompanied by the intracellular calcium and photosensitizer dynamics typical of the effect of PDT on rat epithelial cells. Accordingly, added antioxidants that suppressed light-stimulated proliferation also suppressed this light-stimulated inhibition. The model systems employed in this study are the first to demonstrate the specific effect of PKC isozymes on light-stimulated proliferation, in relation to oxidative stress, and indicate their dual role in light-tissue interaction.
KW - Cultured skin cells
KW - Light-induced proliferation
KW - PKC
KW - Reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=0034586857&partnerID=8YFLogxK
U2 - 10.1117/12.405908
DO - 10.1117/12.405908
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AN - SCOPUS:0034586857
SN - 0277-786X
VL - 4159
SP - 34
EP - 40
JO - Proceedings of SPIE - The International Society for Optical Engineering
JF - Proceedings of SPIE - The International Society for Optical Engineering
ER -