TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization.
TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization.
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DOI：
10.1007/s13238-017-0395-5
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发表时间：
2017-09
期刊：
影响因子：
21.1
通讯作者：
Le Garrec R
中科院分区：
文献类型：
--
作者：
Gouin O;L'Herondelle K;Lebonvallet N;Le Gall-Ianotto C;Sakka M;Buhé V;Plée-Gautier E;Carré JL;Lefeuvre L;Misery L;Le Garrec R
皮肤神经源性炎症（CNI）是通过从感觉神经末梢释放神经肽而在皮肤中诱导（或增强）的炎症。临床表现主要是感觉和血管障碍，如瘙痒和红斑。瞬时受体电位香草酸1和锚蛋白1（分别为TRPV 1和TRPA 1）是已知特异性参与疼痛和CNI的非选择性阳离子通道。TRPV1和TRPA1在感觉神经的大子集中共表达，在那里它们整合了许多伤害性刺激。现在清楚的是，这两种通道的表达也远远超出皮肤中的感觉神经，也发生在角质形成细胞、肥大细胞、树突细胞和内皮细胞中。在这些非神经元细胞中，TRPV1和TRPA1也充当伤害感受器并增强炎症过程。本文综述了TRPV1和TRPA1在调节炎症基因中的作用，这些炎症基因导致或维持感觉神经元和非神经元皮肤细胞中的CNI。此外，本文综述了目前的研究的其他内源性炎症介质，促进CNI的自我维持的TRP通道的细胞内敏化途径的总结。
Cutaneous neurogenic inflammation (CNI) is inflammation that is induced (or enhanced) in the skin by the release of neuropeptides from sensory nerve endings. Clinical manifestations are mainly sensory and vascular disorders such as pruritus and erythema. Transient receptor potential vanilloid 1 and ankyrin 1 (TRPV1 and TRPA1, respectively) are non-selective cation channels known to specifically participate in pain and CNI. Both TRPV1 and TRPA1 are co-expressed in a large subset of sensory nerves, where they integrate numerous noxious stimuli. It is now clear that the expression of both channels also extends far beyond the sensory nerves in the skin, occuring also in keratinocytes, mast cells, dendritic cells, and endothelial cells. In these non-neuronal cells, TRPV1 and TRPA1 also act as nociceptive sensors and potentiate the inflammatory process. This review discusses the role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells. In addition, this review provides a summary of current research on the intracellular sensitization pathways of both TRP channels by other endogenous inflammatory mediators that promote the self-maintenance of CNI.
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DOI：
10.1084/jem.20082242
发表时间：
2009-05-11
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Briot A;Deraison C;Lacroix M;Bonnart C;Robin A;Besson C;Dubus P;Hovnanian A
通讯作者：
Hovnanian A
DOI：
10.1523/jneurosci.3795-08.2008
发表时间：
2008-12-24
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
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作者：
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通讯作者：
Samad TA
DOI：
10.1523/jneurosci.5369-07.2008
发表时间：
2008-03-05
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Andersson DA;Gentry C;Moss S;Bevan S
通讯作者：
Bevan S
影响因子：
2.5
作者：
Anand, U.;Otto, W. R.;Anand, P.
通讯作者：
Anand, P.
DOI：
10.2174/187221312798889266
发表时间：
2012-01-01
影响因子：
4.2
作者：
Andreev, Yaroslav A.;Vassilevski, Alexander A.;Kozlov, Sergey A.
通讯作者：
Kozlov, Sergey A.