Activation of platelet-activating factor receptor in SZ95 sebocytes results in inflammatory cytokine and prostaglandin E2 production

:  Platelet‐activating factor (PAF) is a group of phosphocholines with various biological effects mediated by the PAF receptor (PAF‐R). Activation of the epidermal PAF‐R induces the expression of inflammatory mediators, including cyclooxygenase‐2 (COX‐2) and prostaglandin E2 (PGE2). The upregulation...

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Veröffentlicht in:Experimental dermatology 2006-10, Vol.15 (10), p.769-774
Hauptverfasser: Zhang, Qiwei, Seltmann, Holger, Zouboulis, Christos C., Travers, Jeffrey B.
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Sprache:eng
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Zusammenfassung::  Platelet‐activating factor (PAF) is a group of phosphocholines with various biological effects mediated by the PAF receptor (PAF‐R). Activation of the epidermal PAF‐R induces the expression of inflammatory mediators, including cyclooxygenase‐2 (COX‐2) and prostaglandin E2 (PGE2). The upregulation of COX‐2 expression has been shown to be involved in sebocyte proliferation, sebaceous gland inflammation and carcinogenesis. The present study was designed to investigate whether PAF‐R activation could induce the expression of COX‐2 and production of PGE2, as well as secretion of the inflammatory cytokine, interleukin‐8 (IL‐8), in the immortalized sebaceous gland cell line SZ95. Using calcium mobilization studies, we first confirmed that PAF can signal through PAF‐R in SZ95 sebocytes. We then found that the production of IL‐8 was induced following treatment with PAF‐R agonist, however blocked by a specific PAF‐R antagonist. Induction of COX‐2 expression and increased PGE2 production were observed in SZ95 sebocytes after PAF‐R activation. Finally, it was demonstrated that the production of PGE2, induced by PAF‐R activation and mediated by COX‐2 expression, was blocked following PAF‐R antagonism in SZ95 sebocytes. These studies suggest that SZ95 sebocytes express functional PAF‐Rs and PAF‐Rs are involved in regulating the expression of inflammatory mediators, including COX‐2, PGE2 and IL‐8.
ISSN:0906-6705
1600-0625
DOI:10.1111/j.1600-0625.2006.00458.x