1. ^*Institut für Umweltmedizinische Forschung (IUF) an der Heinrich-Heine-Universität gGmbH, Auf'm Hennekamp 50, D-40225 Duesseldorf, Germany
2. ^†Department of Dermatology, Heinrich-Heine-University, Moorenstr. 5, D-40225 Duesseldorf, Germany
3. ^‡Institut für Physiologische Chemie I, Heinrich-Heine-University, Universitätsstr.1, D-40225 Duesseldorf, Germany
4. ^§Biologisch-Medizinisches Forschungszentrum, Heinrich-Heine-University, Universitätsstr. 1, D-40225 Duesseldorf, Germany

Correspondence: Jean Krutmann, Institut für Umweltmedizinische Forschung (IUF) an der Heinrich-Heine-Universität gGmbH, Auf'm Hennekamp 50, D-40225 Duesseldorf, Germany. Email: krutmann@rz.uni-duesseldorf.de

¹These authors contributed equally to this work.

Received 27 June 2002; Revised 4 September 2002; Accepted 9 September 2002.

Abstract

In addition to ultraviolet radiation, human skin is exposed to infrared radiation from natural sunlight as well as artificial ultraviolet and infrared irradiation devices used for therapeutic or cosmetic purposes. The molecular consequences resulting from infrared exposure are virtually unknown. In this study we have investigated whether infrared has the capacity to affect gene expression in human skin cells. Exposure of cultured human dermal fibroblasts to infrared in the range of 760–1400 nm (infrared-A) induced the expression of matrix metalloproteinase 1 at the mRNA and protein level in a time- and concentration-dependent manner. Expression of tissue inhibitor of matrix metalloproteinase 1 remained unaltered. These effects were not mediated by the generation of heat by infrared-A. Furthermore, infrared-A did not induce heat shock protein 70 expression in human dermal fibroblasts under conditions that increased matrix metalloproteinase 1 expression. Here we provide evidence that infrared-A activated mitogen-activated protein kinase pathways. Extracellular signal-regulated kinase 1/2 and p38-mitogen-activated protein kinase were rapidly activated after infrared-A exposure. The mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor PD 98059, which specifically blocked the extracellular signal-regulated kinase pathway, prevented infrared-A-induced matrix metalloproteinase 1 expression. Upregulation of matrix metalloproteinase 1 expression by infrared-A was thus shown to be dependent on extracellular signal-regulated kinase 1/2 activation. In conclusion, this study demonstrates that infrared-A is capable of inducing matrix metalloproteinase 1 expression in human dermal fibroblasts via activation of the extracellular signal-regulated kinase 1/2 signaling pathway. This previously unrecognized property of infrared-A points to its possible role in the photoaging of human skin.