期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 141, 期 10, 页码 2499-+出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2021.03.015
关键词
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类别
资金
- National Institutes of Health [R01AA027065, R01AR077183, R01DK103901]
- Center for the Study of Itch & Sensory Disorders
- Department of Anesthesiology at Washington University School of Medicine in St. Louis
The study established a sunburn-related mouse model and found that TRPV1-positive dorsal root ganglion neurons are involved in broad-band UVB irradiation induced itch, while mast cells are not. Both genetic and pharmacological inhibition of TRPV1 function significantly alleviated the broad-band UVB irradiation-induced itch response.
Although sunburn can produce severe uncontrollable itching, the underlying mechanisms of UV irradiation induced itch are poorly understood because of a lack of experimental animal models of sunburn itch. In this study, we established a sunburn-related mouse model and found that broad-band UVB irradiation elicited scratching but not wiping behavior in mice. Using a combination of live-cell calcium ion imaging and quantitative RT-PCR on dorsal root ganglion neurons, H&E staining, immunofluorescence staining of skin preparations, and behavioral testing, in combination with genetic and pharmacological approaches, we showed that TRPV1-positive dorsal root ganglion neurons but not mast cells are involved in broad-band UVB irradiation induced itch. Moreover, both genetic and pharmacological inhibition of TRPV1 function significantly alleviated the broad-band UVB irradiation-induced itch response. Collectively, our results suggest that broad-band UVB irradiation evokes itch sensation in mice by promoting TRPV1 channel function in dorsal root ganglion neurons and provide potential therapeutic targets for sunburn-related itch.
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