Induction of manganese superoxide dismutase in human dermal fibroblasts: a UV-B-mediated paracrine mechanism with the release of epidermal interleukin 1 alpha, interleukin 1 beta, and tumor necrosis factor alpha.
BACKGROUND
Reactive oxygen species generated in the skin by UV irradiation promote photoaging and photocarcinogenesis. The manganese (Mn) superoxide dismutase (SOD) is a primary antioxidant enzyme that crucially contributes to the homeostasis of oxygen radicals within the mitochondria, and thus critically participates in the control of senescence and tumor generation.


OBJECTIVE
To determine whether repetitive UV-B exposure, as practiced for light hardening during phototherapy for various photodermatoses, can enhance the adaptive antioxidant response by up-regulating MnSOD activity in either the epidermal or the dermal skin compartment.


METHODS
In vitro experiments to determine MnSOD activity levels in cultured human dermal fibroblasts and epidermal cells (HaCaT cells and primary keratinocytes) at different times after direct UV-B exposure or after incubation of human dermal fibroblasts with supernatants from UV-B-irradiated epidermal cells.


METHODS
Photobiological research laboratory in a university dermatology department.


METHODS
Irradiation of cultured human dermal fibroblasts and epidermal cells with UV-B.


METHODS
Manganese SOD messenger RNA and activity levels in cultured irradiated or mock-treated skin cells.


RESULTS
No increase in MnSOD activity could be detected in fibroblasts or epidermal cells until 24 hours after UV-B irradiation. However, fibroblasts incubated with supernatants from UV-B-irradiated epidermal cells showed a marked increase in specific MnSOD messenger RNA and activity. Removal of interleukin 1alpha, interleukin 1beta, and tumor necrosis factor alpha from the supernatants led to a significant reduction of MnSOD mRNA in fibroblasts.


CONCLUSIONS
Irradiation of the epidermal cells with UV-B induced a release of soluble factors that amplified MnSOD activity in fibroblasts via a paracrine mechanism.
Naderi-Hachtroudi
Lale
L
Department of Dermatology, University of Cologne, Germany.
Peters
Thorsten
T
Brenneisen
Peter
P
Meewes
Christian
C
Hommel
Christina
C
Razi-Wolf
Ziba
Z
Schneider
Lars A
LA
Schüller
Jutta
J
Wlaschek
Meinhard
M
Scharffetter-Kochanek
Karin
K
D002478:Cells, Cultured; D004307:Dose-Response Relationship, Radiation; D000078404:Epidermal Cells; D005347:Fibroblasts / Q000378:metabolism* / Q000528:radiation effects*; D006801:Humans; D007231:Infant, Newborn; D007375:Interleukin-1 / Q000032:analysis; D015603:Keratinocytes / Q000378:metabolism* / Q000528:radiation effects*; D012333:RNA, Messenger / Q000032:analysis*; D012680:Sensitivity and Specificity; D015595:Skin Aging / Q000502:physiology / Q000528:radiation effects*; D013482:Superoxide Dismutase / Q000032:analysis / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014466:Ultraviolet Rays / Q000009:adverse effects*
D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D013482:Superoxide Dismutase