Chen Yong, Moore Carlene D, Zhang Jennifer Y, Hall Russell P, MacLeod Amanda S, Liedtke Wolfgang
Department of Neurology, Duke University, School of Medicine, Durham, North Carolina, USA.
Department of Dermatology, Duke University, Durham, North Carolina, USA.
J Invest Dermatol. 2017 Apr;137(4):801-804. doi: 10.1016/j.jid.2016.12.013.
Mascarenhas et al. report that TRPV4 expression is upregulated in mast cells in response to the proteolytic cathelicidin fragment LL37 in a murine rosacea model and that TRPV4 loss of function attenuates mast cell degranulation. These findings render TRPV4 a translational-medical target in rosacea. However, signaling mechanisms causing increased expression of TRPV4 await elucidation. Moreover, we ask whether TRPV4-mediated Ca-influx evokes mast cell degranulation.
马斯卡雷尼亚斯等人报告称,在小鼠酒渣鼻模型中,瞬时受体电位香草酸亚型4(TRPV4)的表达会因蛋白水解抗菌肽片段LL37而在肥大细胞中上调,并且TRPV4功能丧失会减弱肥大细胞脱颗粒。这些发现使TRPV4成为酒渣鼻的一个转化医学靶点。然而,导致TRPV4表达增加的信号传导机制尚待阐明。此外,我们要问TRPV4介导的钙内流是否会引发肥大细胞脱颗粒。