Cellular response to infrared radiation involves

Cellular response to infrared radiation involves
retrograde mitochondrial signalling
Peter Schroeder, Corinna Pohl, Christian Calles, Corinna Marks, Susanne Wild, Jean Krutmann
Institut für Umweltmedizinische Forschung (IUF) at the Heinrich-Heine-University Düsseldorf gGmbH, Auf ’m Hennekamp 50,
D-40225 Duesseldorf, Germany
Free Radical Biology & Medicine 43 (2007) 128–135
Abstract
Infrared A radiation (IRA) is a major component of sunlight. Similar to ultraviolet (UV) B and
UVA, IRA induces gene transcription. In contrast to the UV response very little is known about
the IRA response. In the present study, IRA-induced expression of matrix metalloproteinase-1
(MMP-1) was found to be mediated by the formation of intracellular reactive oxygen species
(ROS). Staining of IRAirradiated cells with MitoSox revealed an increase in mitochondrial
superoxide anion production and treatment of fibroblasts with the mitochondrial targeted
antioxidant MitoQ completely abrogated the IRA, but not the UVB or UVA1, response. ROS
relevant for IRA-induced signaling originated from the mt electron transport chain, because (i)
chemical inhibition of the electron transport chain prevented IRA, but not UVB or UVA1,
radiation-induced MMP-1 expression, (ii) rho0 fibroblasts specifically failed to increase MMP-1
expression in response to IRA, and (iii) peroxisome proliferator-activated receptor gamma
coactivator-1 (PGC-1) overexpressing fibroblasts with increased electron transport chain
content were hypersensitive to IRA radiation-induced gene expression. Thus, IRA, in contrast to
UV, elicits a retrograde signaling response in human skin.

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