Involvement of Cav3.2 T-type Ca2+ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice

Maho Tsubota; Yuriko Iba; Tsukasa Hatakeyama; Myu Honda; Yoshihito Kasanami; Fumiko Sekiguchi; Atsushi Kawase; Takuya Okada; Naoki Toyooka; Atsufumi Kawabata

doi:10.1016/j.jphs.2024.09.003

Involvement of Ca_v3.2 T-type Ca²⁺ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice

Maho Tsubota, Yuriko Iba, Tsukasa Hatakeyama, Myu Honda, Yoshihito Kasanami, Fumiko Sekiguchi, Atsushi Kawase, Takuya Okada, Naoki Toyooka, Atsufumi Kawabata^*

^*Corresponding author for this work

Life Sciences and Bioengineering

Research output: Contribution to journal › Article › peer-review

Abstract

We tested the hypothesis that Ca_v3.2 T-type Ca²⁺ channels, which can be rebooted by sulfides from Zn²⁺ inhibition under physiological conditions, and sulfide-generating enzymes including cystathionine-β-synthase (CBS) would participate in the colitis-related visceral pain in mice treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). The visceral hypersensitivity following TNBS-induced colitis was abolished by an inhibitor or genetic deletion of Ca_v3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Ca_v3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.

Original language	English
Pages (from-to)	209-213
Number of pages	5
Journal	Journal of Pharmacological Sciences
Volume	156
Issue number	4
DOIs	https://doi.org/10.1016/j.jphs.2024.09.003
State	Published - 2024/12

Keywords

Ca3.2 T-type Ca channel
Colitis-related visceral pain
Cystathionine-β-synthase (CBS)

ASJC Scopus subject areas

Molecular Medicine
Pharmacology

Access to Document

10.1016/j.jphs.2024.09.003

Cite this

@article{3d172aa16a9c4934a7a3650e300d7464,

title = "Involvement of Cav3.2 T-type Ca2+ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice",

abstract = "We tested the hypothesis that Cav3.2 T-type Ca2+ channels, which can be rebooted by sulfides from Zn2+ inhibition under physiological conditions, and sulfide-generating enzymes including cystathionine-β-synthase (CBS) would participate in the colitis-related visceral pain in mice treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). The visceral hypersensitivity following TNBS-induced colitis was abolished by an inhibitor or genetic deletion of Cav3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Cav3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.",

keywords = "Ca3.2 T-type Ca channel, Colitis-related visceral pain, Cystathionine-β-synthase (CBS)",

author = "Maho Tsubota and Yuriko Iba and Tsukasa Hatakeyama and Myu Honda and Yoshihito Kasanami and Fumiko Sekiguchi and Atsushi Kawase and Takuya Okada and Naoki Toyooka and Atsufumi Kawabata",

note = "Publisher Copyright: {\textcopyright} 2024 The Authors",

year = "2024",

month = dec,

doi = "10.1016/j.jphs.2024.09.003",

language = "英語",

volume = "156",

pages = "209--213",

journal = "Journal of Pharmacological Sciences",

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TY - JOUR

T1 - Involvement of Cav3.2 T-type Ca2+ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice

AU - Tsubota, Maho

AU - Iba, Yuriko

AU - Hatakeyama, Tsukasa

AU - Honda, Myu

AU - Kasanami, Yoshihito

AU - Sekiguchi, Fumiko

AU - Kawase, Atsushi

AU - Okada, Takuya

AU - Toyooka, Naoki

AU - Kawabata, Atsufumi

PY - 2024/12

Y1 - 2024/12

N2 - We tested the hypothesis that Cav3.2 T-type Ca2+ channels, which can be rebooted by sulfides from Zn2+ inhibition under physiological conditions, and sulfide-generating enzymes including cystathionine-β-synthase (CBS) would participate in the colitis-related visceral pain in mice treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). The visceral hypersensitivity following TNBS-induced colitis was abolished by an inhibitor or genetic deletion of Cav3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Cav3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.

AB - We tested the hypothesis that Cav3.2 T-type Ca2+ channels, which can be rebooted by sulfides from Zn2+ inhibition under physiological conditions, and sulfide-generating enzymes including cystathionine-β-synthase (CBS) would participate in the colitis-related visceral pain in mice treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). The visceral hypersensitivity following TNBS-induced colitis was abolished by an inhibitor or genetic deletion of Cav3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Cav3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.

KW - Ca3.2 T-type Ca channel

KW - Colitis-related visceral pain

KW - Cystathionine-β-synthase (CBS)

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U2 - 10.1016/j.jphs.2024.09.003

DO - 10.1016/j.jphs.2024.09.003

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AN - SCOPUS:85204530619

SN - 1347-8613

VL - 156

SP - 209

EP - 213

JO - Journal of Pharmacological Sciences

JF - Journal of Pharmacological Sciences

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