MiP2005: Session 11
Mitochondrial Physiology Network 10.9: 129 (2005) - download pdf
A role for mitochondria in infrared A radiation-induced intracellular signalling.
Peter Schroeder, C Marks, S Wild, C Calles, J Krutmann
Cell Biology, Environmental Health Research Institute (IUF), Heinrich-Heine-University, Auf'm Hennekamp 50, D-40225 Duesseldorf. - firstname.lastname@example.org
Infrared-A-radiation (IRA; 760 – 1440 nm) is the major component of natural sunlight and significantly contributes to extrinsic skin ageing. A major hallmark of extrinsic skin ageing is a loss of collagen fibres which results from overexpression of Matrixmetalloproteinase-1 (MMP-1). We have previously shown that IRA radiation is a potent inductor of MMP-1 expression in human dermal fibroblasts. Its effect was shown to be mediated by IRA-induced activation of ERK1/2. Since MAPKinase signalling can be induced by oxidative stress, we aimed to identify whether IRA leads to the formation of ROS, and if yes, whether this would be of functional relevance for IRA-induced gene expression.
Experiments utilizing Mitosox, a dye specific for mitochondrial superoxide radical anions revealed that IRA at physiologically relevant doses leads to an at least threefold increase in O2.-. We have found that IRA induced MMP-1 expression in primary human fibroblasts can be abrogated by mitochondrial respiratory chain inhibitors. This effect was specific since UV-A or UV-B induced MMP-1 expression was not inhibited. In addition we were able to demonstrate, that mitochondria depleted (rho-) cells do not show IRA-induced MMP-1 upregulation in contrast to corresponding rho+ cells. UV-A and UV-B induced MMP-1 induction was not altered by absence of mitochondria.
Taken together our studies for the first time demonstrate that IRA induced gene expression involves retrograde mitochondrial signalling, which seems to be mediated by superoxide radical anions leaking from the respiratory chain.