Involvement of Ca v 3.2 T-type Ca 2+ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice.

Autor: Tsubota M; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Iba Y; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Hatakeyama T; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Honda M; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Kasanami Y; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Sekiguchi F; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Kawase A; Laboratory of Pharmacokinetics, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan., Okada T; Faculty of Engineering, University of Toyama, 3190 Gofuku, Toyama, 930-8555, Japan., Toyooka N; Faculty of Engineering, University of Toyama, 3190 Gofuku, Toyama, 930-8555, Japan., Kawabata A; Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan. Electronic address: kawabata@phar.kindai.ac.jp.
Jazyk: angličtina
Zdroj: Journal of pharmacological sciences [J Pharmacol Sci] 2024 Dec; Vol. 156 (4), pp. 209-213. Date of Electronic Publication: 2024 Sep 21.
DOI: 10.1016/j.jphs.2024.09.003
Abstrakt: We tested the hypothesis that Ca v 3.2 T-type Ca 2+ channels, which can be rebooted by sulfides from Zn 2+ 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 v 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 v 3.2 brought about by sulfides generated by upregulated CBS is involved in the colitis-related visceral hypersensitivity.
Competing Interests: Declaration of competing interest The authors have no conflict of interest regarding this manuscript.
(Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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