title: Infrared radiation confers resistance to UV-induced apoptosis via reduction of DNA damage and upregulation of antiapoptotic proteins.
abstract: Infrared radiation (IR) is increasingly used for wellness purposes. In this setting, it is frequently combined with UV radiation, primarily for tanning purposes. The impact of IR on UV-induced carcinogenesis is still unclear. Hence, we investigated the interplay between IR and UV with regard to UV-induced apoptosis. Pretreatment of murine keratinocytes with IR before UV reduced the apoptotic rate. Likewise, the number of sunburn cells was reduced in mice preexposed to IR before UV. The amounts of UV-induced DNA damage were reduced by IR both in vitro and in vivo. This was not observed in DNA repair-deficient mice. UV-induced downregulation of the antiapoptotic proteins FLIP(L) and BCL-X(L) was prevented by IR, whereas the proapoptotic protein BAX was downregulated. These data indicate that IR reduces UV-induced apoptosis that may be mediated by several pathways, including reduction of DNA damage and induction of antiapoptotic proteins. The antiapoptotic effects of IR may support the survival of UV-damaged cells and thus carcinogenesis. As, however, IR reduces UV-induced DNA damage, the balance between these two effects may be important. Thus, in vivo carcinogenesis studies are required to define the role of IR and its interaction with UV in photocarcinogenesis.
authors.affiliation: Department of Dermatology, University Kiel, Kiel, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Jantschitsch
authors.forename: Sebastian
authors.initials: S
authors.lastname: Majewski
authors.forename: Akira
authors.initials: A
authors.lastname: Maeda
authors.forename: Thomas
authors.initials: T
authors.lastname: Schwarz
authors.forename: Agatha
authors.initials: A
authors.lastname: Schwarz
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D004249:DNA Damage / Q000528:radiation effects*; D053222:Fas Ligand Protein / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D005260:Female; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D007259:Infrared Rays / Q000627:therapeutic use*; D015603:Keratinocytes / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D014466:Ultraviolet Rays / Q000009:adverse effects*; D015854:Up-Regulation / Q000528:radiation effects; D051020:bcl-X Protein / Q000235:genetics / Q000378:metabolism*
chemical_list: C494812:Bcl2l1 protein, mouse; D053446:CASP8 and FADD-Like Apoptosis Regulating Protein; D053222:Fas Ligand Protein; D053200:Fas-Associated Death Domain Protein; D018840:HSP70 Heat-Shock Proteins; D051020:bcl-X Protein