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UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4 ion channels and triggering endothelin-1 signaling.

dc.contributor.author Moore, Carlene
dc.contributor.author Cevikbas, Ferda
dc.contributor.author Pasolli, H Amalia
dc.contributor.author Chen, Yong
dc.contributor.author Kong, Wei
dc.contributor.author Kempkes, Cordula
dc.contributor.author Parekh, Puja
dc.contributor.author Lee, Suk Hee
dc.contributor.author Kontchou, Nelly-Ange
dc.contributor.author Yeh, Iwei
dc.contributor.author Jokerst, Nan Marie
dc.contributor.author Fuchs, Elaine
dc.contributor.author Steinhoff, Martin
dc.contributor.author Liedtke, Wolfgang B
dc.coverage.spatial United States
dc.date.accessioned 2016-10-21T03:03:37Z
dc.date.issued 2013-08-20
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/23929777
dc.identifier 1312933110
dc.identifier.uri https://hdl.handle.net/10161/12972
dc.description.abstract At our body surface, the epidermis absorbs UV radiation. UV overexposure leads to sunburn with tissue injury and pain. To understand how, we focus on TRPV4, a nonselective cation channel highly expressed in epithelial skin cells and known to function in sensory transduction, a property shared with other transient receptor potential channels. We show that following UVB exposure mice with induced Trpv4 deletions, specifically in keratinocytes, are less sensitive to noxious thermal and mechanical stimuli than control animals. Exploring the mechanism, we find that epidermal TRPV4 orchestrates UVB-evoked skin tissue damage and increased expression of the proalgesic/algogenic mediator endothelin-1. In culture, UVB causes a direct, TRPV4-dependent Ca(2+) response in keratinocytes. In mice, topical treatment with a TRPV4-selective inhibitor decreases UVB-evoked pain behavior, epidermal tissue damage, and endothelin-1 expression. In humans, sunburn enhances epidermal expression of TRPV4 and endothelin-1, underscoring the potential of keratinocyte-derived TRPV4 as a therapeutic target for UVB-induced sunburn, in particular pain.
dc.language eng
dc.publisher Proceedings of the National Academy of Sciences
dc.relation.ispartof Proc Natl Acad Sci U S A
dc.relation.isversionof 10.1073/pnas.1312933110
dc.subject calcium-permeable channels
dc.subject epithelial–neuronal cross-talk
dc.subject photodermatitis
dc.subject phototransduction
dc.subject Analysis of Variance
dc.subject Animals
dc.subject Cells, Cultured
dc.subject Endothelin-1
dc.subject Epithelial Cells
dc.subject Immunohistochemistry
dc.subject Mice
dc.subject Mice, Transgenic
dc.subject Microscopy, Electron
dc.subject Pain
dc.subject Signal Transduction
dc.subject Skin
dc.subject Sunburn
dc.subject TRPV Cation Channels
dc.subject Ultraviolet Rays
dc.title UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4 ion channels and triggering endothelin-1 signaling.
dc.type Journal article
duke.contributor.id Moore, Carlene|0494039
duke.contributor.id Chen, Yong|0247728
duke.contributor.id Jokerst, Nan Marie|0311274
duke.contributor.id Liedtke, Wolfgang B|0315649
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/23929777
pubs.begin-page E3225
pubs.end-page E3234
pubs.issue 34
pubs.organisational-group Anesthesiology
pubs.organisational-group Basic Science Departments
pubs.organisational-group Clinical Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Institute for Brain Sciences
pubs.organisational-group Electrical and Computer Engineering
pubs.organisational-group Institutes and Provost's Academic Units
pubs.organisational-group Neurobiology
pubs.organisational-group Neurology
pubs.organisational-group Neurology, Headache and Pain
pubs.organisational-group Pratt School of Engineering
pubs.organisational-group School of Medicine
pubs.organisational-group University Institutes and Centers
pubs.publication-status Published
pubs.volume 110
dc.identifier.eissn 1091-6490
duke.contributor.orcid Moore, Carlene|0000-0002-1468-6408
duke.contributor.orcid Liedtke, Wolfgang B|0000-0003-4166-5394


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