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低渗诱导的细胞肿胀激活瞬时受体电位锚蛋白1（TRPA1）。

Hypotonicity-induced cell swelling activates TRPA1.

作者信息

Fujita Fumitaka, Uchida Kunitoshi, Takayama Yasunori, Suzuki Yoshiro, Takaishi Masayuki, Tominaga Makoto

机构信息

Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences, Okazaki, Aichi, 444-8787, Japan.

Basic Research Institute, Mandom Corp., Osaka, 540-8530, Japan.

出版信息

J Physiol Sci. 2018 Jul;68(4):431-440. doi: 10.1007/s12576-017-0545-9. Epub 2017 Jun 16.

DOI:10.1007/s12576-017-0545-9
PMID:28623463
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6351518/
Abstract

Hypotonic solutions can cause painful sensations in nasal and ocular mucosa through molecular mechanisms that are not entirely understood. We clarified the ability of human TRPA1 (hTRPA1) to respond to physical stimulus, and evaluated the response of hTRPA1 to cell swelling under hypotonic conditions. Using a Ca-imaging method, we found that modulation of AITC-induced hTRPA1 activity occurred under hypotonic conditions. Moreover, cell swelling in hypotonic conditions evoked single-channel activation of hTRPA1 in a cell-attached mode when the patch pipette was attached after cell swelling under hypotonic conditions, but not before swelling. Single-channel currents activated by cell swelling were also inhibited by a known hTRPA1 blocker. Since pre-application of thapsigargin or pretreatment with the calcium chelator BAPTA did not affect the single-channel activation induced by cell swelling, changes in intracellular calcium concentrations are likely not related to hTRPA1 activation induced by physical stimuli.

摘要

低渗溶液可通过尚未完全明确的分子机制在鼻黏膜和眼黏膜中引发疼痛感。我们阐明了人类瞬时受体电位锚蛋白1（hTRPA1）对物理刺激的响应能力，并评估了hTRPA1在低渗条件下对细胞肿胀的反应。采用钙成像方法，我们发现低渗条件下异硫氰酸烯丙酯（AITC）诱导的hTRPA1活性发生了调节。此外，在低渗条件下细胞肿胀后连接膜片移液器时，低渗条件下的细胞肿胀会以细胞贴附模式诱发hTRPA1的单通道激活，但在肿胀前连接则不会。细胞肿胀激活的单通道电流也受到已知的hTRPA1阻滞剂的抑制。由于预先应用毒胡萝卜素或用钙螯合剂BAPTA预处理不影响细胞肿胀诱导的单通道激活，细胞内钙浓度的变化可能与物理刺激诱导的hTRPA1激活无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/30022851befe/12576_2017_545_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/439a6ea70846/12576_2017_545_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/aa8f3271d1e0/12576_2017_545_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/782847b84034/12576_2017_545_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/e15045e372fc/12576_2017_545_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/670d94428006/12576_2017_545_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/d914fb4a0793/12576_2017_545_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/30022851befe/12576_2017_545_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/439a6ea70846/12576_2017_545_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/aa8f3271d1e0/12576_2017_545_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/782847b84034/12576_2017_545_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/e15045e372fc/12576_2017_545_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/670d94428006/12576_2017_545_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/d914fb4a0793/12576_2017_545_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a30/10717182/30022851befe/12576_2017_545_Fig7_HTML.jpg

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本文引用的文献

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TNF-α-induced p38MAPK activation regulates TRPA1 and TRPV4 activity in odontoblast-like cells.TNF-α 诱导的 p38MAPK 激活调节成牙本质细胞样细胞中的 TRPA1 和 TRPV4 活性。
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TRPM8 is a neuronal osmosensor that regulates eye blinking in mice.
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Calcium-dependent, non-apoptotic, large plasma membrane bleb formation in physiologically stimulated mast cells and basophils.在生理刺激的肥大细胞和嗜碱性粒细胞中，钙依赖性、非凋亡性的大质膜泡形成。
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