UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4 ion channels and triggering endothelin-1 signaling.
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.
Type
Journal articleSubject
calcium-permeable channelsepithelial–neuronal cross-talk
photodermatitis
phototransduction
Analysis of Variance
Animals
Cells, Cultured
Endothelin-1
Epithelial Cells
Immunohistochemistry
Mice
Mice, Transgenic
Microscopy, Electron
Pain
Signal Transduction
Skin
Sunburn
TRPV Cation Channels
Ultraviolet Rays
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https://hdl.handle.net/10161/12972Published Version (Please cite this version)
10.1073/pnas.1312933110Publication Info
Moore, Carlene; Cevikbas, Ferda; Pasolli, H Amalia; Chen, Yong; Kong, Wei; Kempkes,
Cordula; ... Liedtke, Wolfgang B (2013). UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4
ion channels and triggering endothelin-1 signaling. Proc Natl Acad Sci U S A, 110(34). pp. E3225-E3234. 10.1073/pnas.1312933110. Retrieved from https://hdl.handle.net/10161/12972.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Yong Chen
Associate Professor in Neurology
Nan Marie Jokerst
J. A. Jones Distinguished Professor of Electrical and Computer Engineering
Dr. Nan Marie Jokerst is the J. A. Jones Distinguished Professor of Electrical and
Computer Engineering at Duke University, and the Executive Director of the Duke Shared
Materials Instrumentation Facility, a Duke shared cleanroom and characterization facility.
She received her BS in Physics from Creighton University in 1982, and her MS and
PhD in Electrical Engineering from the University of Southern California in 1984 and
1989, respectively. She is a Fellow of the IEEE, and has served as an el
Wolfgang Bernhard Liedtke
Adjunct Professor in the Department of Neurology
Research Interests in the Liedtke-Lab:
Pain/ nociception
Sensory transduction and -transmission
TRP ion channels
Water and salt equilibrium regulated by the central nervous system
Visit the lab's website, download papers and read Dr. Liedtke's CV here.
Carlene D Moore
Assistant Professor in Neurology
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