The Platelet-activating Factor Receptor Protects Epidermal Cells from Tumor Necrosis Factor (TNF) α and TNF-related Apoptosis-inducing Ligand-induced Apoptosis through an NF-κB-dependent Process
dc.contributor.author | Southall, Michael D. | |
dc.contributor.author | Isenberg, Jason S. | |
dc.contributor.author | Nakshatri, Harikrishna | |
dc.contributor.author | Yi, Qiaofang | |
dc.contributor.author | Pei, Yong | |
dc.contributor.author | Spandau, Dan F. | |
dc.contributor.author | Travers, Jeffrey B. | |
dc.date.accessioned | 2019-04-10T21:11:34Z | |
dc.date.available | 2019-04-10T21:11:34Z | |
dc.date.issued | 2001-12-07 | |
dc.description.abstract | A number of chemical mediators can induce human keratinocytes and epidermal-derived carcinomas to undergo apoptosis, or programmed cell death. Recent evidence suggests pro-inflammatory cytokines, such as interleukin-1β or transforming growth factor α, protects carcinomas from numerous pro-apoptotic stimuli. Platelet-activating factor (1-alkyl-2-acetyl-3-glycerophosphocholine; PAF) is a lipid mediator with pro-inflammatory effects on numerous cell types. Although PAF can be metabolized to other bioactive lipids, the majority of PAF effects occur through activation of a G protein-coupled receptor. Using a model system created by retroviral transduction of the PAF receptor (PAF-R) into the PAF-R-negative human epidermal cell line KB and the PAF-R-expressing keratinocyte cell line HaCaT, we now demonstrate that activation of the epidermal PAF-R results in protection from apoptosis induced by tumor necrosis factor (TNF) α or TNF-related apoptosis-inducing ligand. The PAF-mediated protection was inhibited by PAF-R antagonists, and protection did not occur in PAF-R-negative KB cells. Additionally, we show protection from TNFα- or TRAIL-induced apoptosis by PAF-R activation is dependent on the transcription factor nuclear factor (NF)-κB, because PAF-R activation-induced NF-κB and epidermal cells transduced with a super-repressor form of inhibitor κB were not protected by the PAF-R. These studies provide a mechanism whereby the epidermal PAF-R, and possibly other G protein-coupled receptors, can exert anti-apoptotic effects through an NF-κB-dependent process. | en_US |
dc.identifier.citation | Southall, M. D., Isenberg, J. S., Nakshatri, H., Yi, Q., Pei, Y., Spandau, D. F., & Travers, J. B. (2001). The Platelet-activating Factor Receptor Protects Epidermal Cells from Tumor Necrosis Factor (TNF) α and TNF-related Apoptosis-inducing Ligand-induced Apoptosis through an NF-κB-dependent Process. Journal of Biological Chemistry, 276(49), 45548–45554. https://doi.org/10.1074/jbc.M105978200 | en_US |
dc.identifier.doi | 10.1074/jbc.M105978200 | |
dc.identifier.issn | 0021-9258, 1083-351X | |
dc.identifier.uri | https://hdl.handle.net/1805/18816 | |
dc.language.iso | en_US | en_US |
dc.publisher | American Society for Biochemistry and Molecular Biology | en_US |
dc.subject | Epidermal Cells | en_US |
dc.subject | Platelets | en_US |
dc.subject | Tumor Necrosis Factor | en_US |
dc.title | The Platelet-activating Factor Receptor Protects Epidermal Cells from Tumor Necrosis Factor (TNF) α and TNF-related Apoptosis-inducing Ligand-induced Apoptosis through an NF-κB-dependent Process | en_US |
dc.type | Article | en_US |
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