UVB radiation generates sunburn pain and affects skin by activating epidermal TRPV4 ion channels and triggering endothelin-1 signaling.
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2013-08-20
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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.
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Moore, Carlene, Ferda Cevikbas, H Amalia Pasolli, Yong Chen, Wei Kong, Cordula Kempkes, Puja Parekh, Suk Hee Lee, et al. (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.
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Scholars@Duke
Carlene D Moore
Yong Chen
Dr. Yong Chen is an Associate Professor of Neurology at the Duke University School of Medicine. He is also affiliated with Duke Anesthesiology-Center for Translational Pain Medicine (CTPM) and Duke-Pathology.
The Chen lab mainly studies sensory neurobiology of pain and itch, with a focus on TRP ion channels and neural circuits. The main objective of our lab is to identify molecular and cellular mechanisms underlying chronic pain and chronic-disease associated itch, using a combination of animal behavioral, genetic, molecular and cellular, advanced imaging, viral, and optogenetic approaches. There are three major research areas in the lab: craniofacial pain, arthritis pain and joint function, and systemic-disease associated itch.
Nan Marie Jokerst
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 was the Chair of the Duke Academic Council from 2014-2015 and an Associate Dean in the Pratt School of Engineering for 6 years. 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 elected member of the IEEE Photonics Board of Governors, and as the VP for Conferences and as the VP Technical Affairs, as well as the Atlanta Section President, Vice President, Treasurer, and Secretary, and a member of the IEEE Proceedings Editorial Board. She is a Fellow of Optica (formerly the the Optical Society of America), and has served as Chair of the OSA Engineering Council and as an Associate Editor of Optica. Her awards include an NSF Presidential Young Investigator Award, an IEEE Third Millenium Medal, the IEEE/HP Harriet B. Rigas Medal, and the Alumni in Academia Award for the University of Southern California Viterbi School of Engineering. She also served on the National Academies Board on Global Science and Technology. She has published over 250 refereed journal and conference publications, and has 6 patents. She is a co-founder of the organization Triangle Women in STEM.
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