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Wound Repair Regen. 2016 Sep;24(5):841-850. doi: 10.1111/wrr.12469.

Increased activity of TRPV3 in keratinocytes in hypertrophic burn scars with postburn pruritus.

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Department of Dermatology, Hallym University, Seoul, Korea.
Department of Anesthesiology and Pain Medicine, College of Medicine, Hallym University, Seoul, Korea.
Department of Computer Science, Kwangwoon University, Seoul, Korea, and.
Department of Dermatology, The Catholic University of Korea, Seoul, Korea.


Postburn pruritus is a common distressing sequela of burn wounds. Empirical antipruritic treatment often fails to have a satisfactory outcome, as the mechanism of it has not been fully elucidated. The aim of this study was to evaluate the manifestation of transient receptor potential vanilloid 3 (TRPV3), transient receptor potential ankyrin 1 (TRPA1), and other related receptors in postburn pruritus. Sixty-five burn patients with (n = 40) or without (n = 25) pruritus were investigated, including skin biopsies. Keratinocytes and fibroblasts from skin biopsy samples were separated. Real time-PCR showed that mRNA of TRPV3 was significantly increased in keratinocytes from pruritic burn scars than in keratinocytes from nonpruritic burn scars. With TRPV3 activation, intracellular Ca2+ concentrations were more significantly increased in keratinocytes from pruritic burn scars than in those from nonpruritic ones. Additionally, mRNA and protein levels of protease-activated receptor 2 (PAR2) and neurokinin-1 receptor (NK1R) were also significantly increased in pruritic burn scars. In conclusion, it was confirmed that TRPV3, PAR2, and NK1R were highly expressed in pruritic burn scars. These results may help determine a novel mechanism for postburn pruritus.


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