UVB Generates Microvesicle Particle Release in Part Due to Platelet-activating Factor Signaling

The lipid mediator platelet‐activating factor (PAF) and oxidized glycerophosphocholine PAF agonists produced by ultraviolet B (UVB) have been demonstrated to play a pivotal role in UVB‐mediated processes, from acute inflammation to delayed systemic immunosuppression. Recent studies have provided evidence that microvesicle particles (MVPs) are released from cells in response to various signals including stressors. Importantly, these small membrane fragments can interact with various cell types by delivering bioactive molecules. The present studies were designed to test if UVB radiation can generate MVP release from epithelial cells, and the potential role of PAF receptor (PAF‐R) signaling in this process. We demonstrate that UVB irradiation of the human keratinocyte‐derived cell line HaCaT resulted in the release of MVPs. Similarly, treatment of HaCaT cells with the PAF‐R agonist carbamoyl PAF also generated equivalent amounts of MVP release. Of note, pretreatment of HaCaT cells with antioxidants blocked MVP release from UVB but not PAF‐R agonist N‐methyl carbamyl PAF (CPAF). Importantly, UVB irradiation of the PAF‐R‐negative human epithelial cell line KB and KB transduced with functional PAF‐Rs resulted in MVP release only in PAF‐R‐positive cells. These studies demonstrate that UVB can generate MVPs in vitro and that PAF‐R signaling appears important in this process. In this study, we demonstrated that ultraviolet B (UVB) radiation generates microvesicle particles (MVP) release from epithelial cells. We have discovered that activation of the keratinocyte platelet‐activating factor receptor (PAF‐R) results in MVP release, and using an epithelial cell line with/without PAF‐Rs, we demonstrate that UVB generates MVP via PAF‐R signaling. Importantly, UVB‐generated PAF agonist formation and MVP release are blocked by antioxidants. Yet, antioxidants do not affect MVP release in response to a PAF agonist. This study suggests that UVB generates MVP release from epithelial cells, which could provide a potential mechanism for UVB‐mediated systemic signaling.