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

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Title: IL-1 beta augments H2S-induced increase in intracellular Ca2+ through polysulfides generated from H2S/NO interaction
Authors: Ujike, Ayako Browse this author
Kuraishi, Tomoki Browse this author
Yamaguchi, Soichiro Browse this author →KAKEN DB
Eguchi, Ryota Browse this author
Kitano, Taisuke Browse this author
Kamise, Jumpei Browse this author
Ito, Shigeo Browse this author →KAKEN DB
Otsuguro, Ken-ichi Browse this author →KAKEN DB
Keywords: Hydrogen sulfide
Polysulfide
TRPA1
K-ATP channels
IL-1 beta
NO
Issue Date: 15-Feb-2018
Publisher: Elsevier
Journal Title: European journal of pharmacology
Volume: 821
Start Page: 88
End Page: 96
Publisher DOI: 10.1016/j.ejphar.2018.01.006
PMID: 29337193
Abstract: 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.
Rights: © 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/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/72833
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 乙黒 兼一

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