Involvement of platelet-activating factor in ultraviolet B-induced hyperalgesia.

Qiwei Zhang, Leslie A. Sitzman, Mohammad Al-Hassani, Shanbao Cai, Karen Pollok, Jeffrey Travers, Cynthia M. Hingtgen

Research output: Contribution to journalArticle

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Abstract

Ultraviolet B (UVB) radiation causes cutaneous inflammation. One important clinical consequence of UVB-induced inflammation is increased pain or hyperalgesia, which is likely mediated by enhanced sensitivity of cutaneous sensory neurons. Previous studies have demonstrated that UVB radiation generates the lipid mediator, platelet-activating factor (PAF), as well as oxidized phospholipids that act as PAF-mimetics. These substances exert effects through the PAF receptor (PAF-R). This study was designed to assess whether PAF-R is involved in UVB-induced hyperalgesia. Intradermal injection of carbamoyl PAF (CPAF; 1-hexadecyl-2-N-methylcarbamoyl glycerophosphocholine) resulted in an enhanced response to mechanical stimuli in wild-type mice but not in PAF-R knockout (KO) mice. There was no significant change in paw withdrawal to noxious thermal stimuli in either genotype after intradermal injection of CPAF. Exposure of the hind paw to 1,500 J m(-2) UVB radiation caused an increased sensitivity to both mechanical and thermal stimulation in wild-type mice but not in PAF-R KO mice. The thermal hyperalgesia caused by UVB irradiation was inhibited in mice that lacked PAF-R in bone marrow-derived cells. These data demonstrate that the PAF-R is important for UVB-induced hyperalgesia. Further investigation of the role of PAF-R signaling in UVB-induced hyperalgesia could provide better understanding of the pathological processes initiated by UVB-induced skin damage.

Original languageEnglish
Pages (from-to)167-174
Number of pages8
JournalJournal of Investigative Dermatology
Volume129
Issue number1
DOIs
StatePublished - Jan 2009

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Platelet Activating Factor
Hyperalgesia
Intradermal Injections
Radiation
Knockout Mice
Skin
Hot Temperature
Inflammation
Sensory Receptor Cells
Pathologic Processes
Bone Marrow Cells
Neurons
Phospholipids
Bone
Genotype
Irradiation
Lipids
Pain

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Involvement of platelet-activating factor in ultraviolet B-induced hyperalgesia. / Zhang, Qiwei; Sitzman, Leslie A.; Al-Hassani, Mohammad; Cai, Shanbao; Pollok, Karen; Travers, Jeffrey; Hingtgen, Cynthia M.

In: Journal of Investigative Dermatology, Vol. 129, No. 1, 01.2009, p. 167-174.

Research output: Contribution to journalArticle

Zhang, Qiwei ; Sitzman, Leslie A. ; Al-Hassani, Mohammad ; Cai, Shanbao ; Pollok, Karen ; Travers, Jeffrey ; Hingtgen, Cynthia M. / Involvement of platelet-activating factor in ultraviolet B-induced hyperalgesia. In: Journal of Investigative Dermatology. 2009 ; Vol. 129, No. 1. pp. 167-174.
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abstract = "Ultraviolet B (UVB) radiation causes cutaneous inflammation. One important clinical consequence of UVB-induced inflammation is increased pain or hyperalgesia, which is likely mediated by enhanced sensitivity of cutaneous sensory neurons. Previous studies have demonstrated that UVB radiation generates the lipid mediator, platelet-activating factor (PAF), as well as oxidized phospholipids that act as PAF-mimetics. These substances exert effects through the PAF receptor (PAF-R). This study was designed to assess whether PAF-R is involved in UVB-induced hyperalgesia. Intradermal injection of carbamoyl PAF (CPAF; 1-hexadecyl-2-N-methylcarbamoyl glycerophosphocholine) resulted in an enhanced response to mechanical stimuli in wild-type mice but not in PAF-R knockout (KO) mice. There was no significant change in paw withdrawal to noxious thermal stimuli in either genotype after intradermal injection of CPAF. Exposure of the hind paw to 1,500 J m(-2) UVB radiation caused an increased sensitivity to both mechanical and thermal stimulation in wild-type mice but not in PAF-R KO mice. The thermal hyperalgesia caused by UVB irradiation was inhibited in mice that lacked PAF-R in bone marrow-derived cells. These data demonstrate that the PAF-R is important for UVB-induced hyperalgesia. Further investigation of the role of PAF-R signaling in UVB-induced hyperalgesia could provide better understanding of the pathological processes initiated by UVB-induced skin damage.",
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