Biochemical and Biophysical Research Communications
Influence of TRPV3 mutation on hair growth cycle in mice
Section snippets
Materials and methods
Animals. DS-Nh mice were originally derived from a colony of an inbreed DS strain in 1976. DS mice were developed from an outbreed ddN stock obtained in 1954 from the Central Institute for Experimental Animals, Tokyo, Japan. DS and DS-Nh mice were maintained at Aburahi Laboratories, Shionogi & Co., Ltd., Shiga, Japan. They were kept in micro-isolator cages in SPF animal rooms, and exposed to a 12 h light/12 h dark cycle while provided with standard feed and water ad libitum. The study was
Results and discussion
We measured Ca2+ influx into epidermal sheets from both strains to elucidate the thermal susceptibility caused by mutation of TRPV3 (Fig. 1A). Ca2+ influx into epidermal sheets from DS-Nh mice was detected at a lower temperature than that from DS mice. Interestingly, Xiao et al. [13] speculated that Gly573Ser substituted TRPV3 was spontaneously active in vivo and normal physiological conditions. Furthermore, DS-Nh mice spontaneously develop a hairless phenotype with an autosomal dominant
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Molecular determinants for the chemical activation of the warmth-sensitive TRPV3 channel by the natural monoterpenoid carvacrol
2022, Journal of Biological ChemistryHair Loss Caused by Gain-of-Function Mutant TRPV3 Is Associated with Premature Differentiation of Follicular Keratinocytes
2021, Journal of Investigative DermatologyCitation Excerpt :The Trpv3 knock-in mouse models reported in this study recapitulated the hair loss of OS both genetically and phenotypically, suggesting that the pathogenesis underlying hair loss in these mouse models is likely parallel to that of patients with OS. Moreover, the DS-Nh mice (Asakawa et al., 2006; Imura et al., 2007), which harbor a dominant mutant Trpv3 (G573S), exhibited hair phenotypes that were, to a large extent, similar to those observed in the Trpv3 knock-in mouse models described in this paper, confirming the detrimental effect of dominant mutant Trpv3 on hair formation. The HF phenotypes in Trpv3 knock-in mice temporally and spatially correlated with the expression profile of Trpv3 and severely affected the differentiation events of KCs in the IRS and hair shaft compartments.
TRPV3 expression and purification for structure determination by Cryo-EM
2021, Methods in EnzymologyCitation Excerpt :Its expression has also been detected in corneal epithelial cells (Yamada et al., 2010) and the distal colon epithelium (Ueda, Yamada, Ugawa, Ishida, & Shimada, 2009). TRPV3 is implicated in cutaneous sensation, including thermo-sensation (Chung, Lee, Mizuno, Suzuki, & Caterina, 2004a; Mandadi et al., 2009; Moqrich et al., 2005; Peier et al., 2002; Smith et al., 2002; Xu et al., 2002), nociception and itch (Cui, Wang, Wei, & Wang, 2018; Yamamoto-Kasai et al., 2012; Zhao et al., 2020), in addition to maintenance of the skin barrier and wound healing (Aijima et al., 2015; Miyamoto, Petrus, Dubin, & Patapoutian, 2011; Yamada et al., 2010), hair growth (Asakawa et al., 2006; Cheng et al., 2010; Imura et al., 2007), and embryonic development (Carvacho, Lee, Fissore, & Clapham, 2013). The dysfunction of TRPV3 channels is associated with numerous human diseases, including a genodermatosis known as Olmsted syndrome (Duchatelet et al., 2014; Lin et al., 2012; Ni et al., 2016), atopic dermatitis (Qu, Wang, Sun, & Wang, 2019), dermal fibrosis (Um et al., 2020), cardiac hypertrophy (Zhang et al., 2018), and rosacea (Sulk et al., 2012).
Activation of TRPV3 Regulates Inflammatory Actions of Human Epidermal Keratinocytes
2018, Journal of Investigative DermatologyCitation Excerpt :Recent research has shown that various mutations of the TRPV3 gene are the underlying cause of both the phenotype of DS-Nh mice and for Olmsted syndrome, a serious cutaneous condition characterized by palmoplantar keratoderma, periorifacial hyperkeratosis, diffuse hypotrichosis and alopecia, and itch (Asakawa et al., 2006; Lin et al., 2012). Previous reports on TRPV3 have centered around observations in mice, where it has been described that (i) the gain-of-function mutation of TRPV3 shows higher Ca2+ incorporation and nerve growth factor production compared with DS mice without the mutation (Imura et al., 2007; Yoshioka et al., 2009), (ii) 2-APB (an activator of TRPV3 we used in this study) activates keratinocytes from DS-Nh mice at lower concentrations than control keratinocytes, and (iii) TRPV3 activation leads to TSLP secretion in DS-Nh mice using TRPV3-knockout mice as control (Yamamoto-Kasai et al., 2013). TRPV3 expression has also been shown to be increased in keratinocytes of atopic dermatitis (hence most probably inflamed) lesions (Yamamoto-Kasai et al., 2013).
Role of TRP Channels in Skin Diseases
2015, TRP Channels as Therapeutic Targets: From Basic Science to Clinical Use