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

We tested the hypothesis that Ca<sub>v</sub>3.2 T-type Ca<sup>2+</sup> channels, which can be rebooted by sulfides from Zn<sup>2+</sup> 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<sub>v</sub>3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Ca<sub>v</sub>3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.

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Journal
Journal of Pharmacological Sciences
Published
2024-09-21
DOI
https://doi.org/10.1016/j.jphs.2024.09.003
Primary Topic
Sulfur Compounds in Biology
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article
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article

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

Naoki Toyooka, Yuriko Iba, Fumiko Sekiguchi, Atsushi Kawase et al.
Journal of Pharmacological Sciences
Sulfur Compounds in Biology
article

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

Naoki Toyooka, Yuriko Iba, Fumiko Sekiguchi, Atsushi Kawase, Atsufumi Kawabata, Takuya Okada, Yoshihito Kasanami, Maho Tsubota, M. HONDA, T Hatakeyama
article en

Abstract

We tested the hypothesis that Ca<sub>v</sub>3.2 T-type Ca<sup>2+</sup> channels, which can be rebooted by sulfides from Zn<sup>2+</sup> 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<sub>v</sub>3.2 and by a CBS inhibitor, and accompanied by CBS upregulation in the colon. Our data thus suggest that the enhanced activity of Ca<sub>v</sub>3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.

Journal of Pharmacological SciencesVol. 156(4)
University of Toyama (JP), Kindai University (JP)
Openalex Percentile: Top 84%
Sulfur Compounds in Biology
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