Pathophysiological analysis of oral diseases caused by dysregulation of cation channels

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K11036
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Functional basic dentistry
• Research Institution: Tohoku University
• Principal Investigator: Wakamori Minoru 東北大学, 歯学研究科, 教授 (50222401)
• Co-Investigator(Kenkyū-buntansha): 吉田 卓史 東北大学, 歯学研究科, 助教 (30455795) ; 高橋 哲 東北大学, 歯学研究科, 教授 (60226850) ; 熊本 裕行 東北大学, 歯学研究科, 教授 (70215028) ; 窪田 寿彦 東北大学, 歯学研究科, 助教 (80377746)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: TRP / チャネル

Outline of Final Research Achievements

We studied the effects of the stimulating ingredients on TRPA1 channel recombinantly expressed in HEK293 cells using the Ca2+ imaging analysis and the patch-clamp technique. Formaldehyde, butylaldehyde, methyl ethyl ketone, and NNK (4-(methylnitrosoamino) -1-(3-pyridyl)-1-butanoe) activated TRPA1 channel, although acetone, crotonaldyhyde, isoprene, and nicotine did not induce Ca2+ transient. Acrylonitrile induced TRPA1 channel current.
We examined the responses to the cigarette smoke elements in trigeminal ganglion neurons and human gingival fibroblast 1. TRPA1 channel was expressed in TRG neurons and HGF-1 cells. Similar to the selective TRPA1 agonist allyl isothiocyanate (AITC), the chemical substances contained in the smoke of tobacco increased intracellular Ca2+ concentration, and induced the outwardly rectifying currents. The responses were blocked by the selective TRPA1 antagonist HC-030031. Therefore it is suggested that TRPA1 channel is activated by the ingredients.

Free Research Field

歯科薬理学