Inhibition of 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] binding to epidermal cells by ultraviolet-B.
12-hydroxyeicosatetraenoic acid (12-HETE), the main eicosanoid in skin, is assumed to have both pathophysiologic effects in inflammatory skin diseases such as psoriasis and atopic eczema and a physiologic role in the biology of cutaneous reparative processes. Because 12-HETE exerts its effects via specific high-affinity epidermal receptors, and ultraviolet-B (UV-B) is capable of modulating various cell-surface molecules, the effects of single and repeated UV-B irradiations on the 12(S)-HETE binding sites in a human epidermal cell line, SCL-II, were studied. UV-B (100-300 J/m2) induced a large decrease in 12(S)-HETE binding in a dose-dependent manner. The inhibition occurred after a latency period of 6 h, reached its maximum at 18 h and slowly declined thereafter. A single UV-B dose of 300 J/m2 or repeated irradiation with 50 J/m2 of UV-B resulted in a 70% decrease in the number of binding sites (Bmax), whereas receptor affinity remained unaffected. The modulation of epidermal 12-HETE receptors by UV-B may partly explain the therapeutic effects of UV-B, but possibly also contribute to photodamage to skin.
Kemény
L
L
Department of Dermatology, University of Munich, F.R.G.
Przybilla
B
B
Gross
E
E
Arenberger
P
P
Ruzicka
T
T
D002452:Cell Count / Q000528:radiation effects; D004305:Dose-Response Relationship, Drug; D004817:Epidermis / Q000648:ultrastructure; D006801:Humans; D011956:Receptors, Cell Surface / Q000528:radiation effects*; D018055:Receptors, Eicosanoid; D013997:Time Factors; D014407:Tumor Cells, Cultured / Q000528:radiation effects; D014466:Ultraviolet Rays
C066652:12-hydroxyeicosatetraenoic acid receptor; D011956:Receptors, Cell Surface; D018055:Receptors, Eicosanoid