IL-1 beta augments H2S-induced increase in intracellular Ca2+ through polysulfides generated from H2S/NO interaction

Ujike, Ayako; Kuraishi, Tomoki; Yamaguchi, Soichiro; Eguchi, Ryota; Kitano, Taisuke; Kamise, Jumpei; Ito, Shigeo; Otsuguro, Ken-ichi

IL-1 beta augments H2S-induced increase in intracellular Ca2+ through polysulfides generated from H2S/NO interaction

Ujike, Ayako; Kuraishi, Tomoki; Yamaguchi, Soichiro et al.

European journal of pharmacology, 2018, 821, 88-96

Permalink : https://hdl.handle.net/2115/72833

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論文情報

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アクセス権	open access
URI	https://hdl.handle.net/2115/72833
タイトル	IL-1 beta augments H2S-induced increase in intracellular Ca2+ through polysulfides generated from H2S/NO interaction
著者	Ujike, Ayako ; Kuraishi, Tomoki ; Yamaguchi, Soichiro ; Eguchi, Ryota ; Kitano, Taisuke ; Kamise, Jumpei ; Ito, Shigeo ; Otsuguro, Ken-ichi
著者名 Ujike, Ayako
著者名 Kuraishi, Tomoki
e-Rad_Researcher 50596864 著者名 Yamaguchi, Soichiro
著者名 Eguchi, Ryota
著者名 Kitano, Taisuke
著者名 Kamise, Jumpei
e-Rad_Researcher 40109509 著者名 Ito, Shigeo
e-Rad_Researcher 40344494 著者名 Otsuguro, Ken-ichi
言語	英語
キーワード	Hydrogen sulfide
	Polysulfide
	TRPA1
	K-ATP channels
	IL-1 beta
	NO
発行日	2018-02-15
出版者	Elsevier
収録物名	European journal of pharmacology
巻(号)	821
ページ	88-96
抄録	H2S has excitatory and inhibitory effects on Ca2+ signals via transient receptor potential ankyrin 1 (TRPA1) and ATP-sensitive K+ channels, respectively. H2S converts intracellularly to polysulfides, which are more potent agonists for TRPA1 than H2S. Under inflammatory conditions, changes in the expression and activity of these H2S target channels and/or the conversion of H2S to polysulfides may modulate H2S effects. Effects of proinflammatory cytokines on H2S-induced Ca2+ signals and polysulfide production in RIN14B cells were examined using fluorescence imaging with fura-2 and SSP4, respectively. Na2S, a H2S donor, induced 1) the inhibition of spontaneous Ca2+ signals, 2) inhibition followed by [Ca2+](i) increase, and 3) rapid [Ca2+](i) increase without inhibition in 50% (23/46), 22% (10/46), and 17% (8/46) of cells tested, respectively. IL-1 beta augmented H2S-induced [Ca2+](i) increases, which were inhibited by TRPA1 and voltage-dependent L-type Ca2+ channel blockers. However, IL-1 beta treatment did not affect [Ca2+](i) increases evoked by a TRPA1 agonist or high concentration of KCl. Na2S increased intracellular polysulfide levels, which were enhanced by IL-1 beta treatment. A NOS inhibitor suppressed the increased polysulfide production and [Ca2+](i) increase in IL-1 beta-treated cells. These results suggest that IL-1 beta augments H2S-induced [Ca2+](i) increases via the conversion of H2S to polysulfides through NO synthesis, but not via changes in the activity and expression of target channels. Polysulfides may play an important role in the effects of H2S during inflammation.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
権利情報	Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
権利情報	© 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
PISSN	0014-2999
関連情報	PMID 29337193
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1016/j.ejphar.2018.01.006