S3-2 Roles of the hydrogen sulfide-CAV3.2 T-type calcium channel pathway in neuronal and neuroendocrine differentiation

Nitric Oxide ◽  
2014 ◽  
Vol 39 ◽  
pp. S3
Author(s):  
Atsufumi Kawabata
Keyword(s):  
Hydrogen Sulfide ◽  
Calcium Channel ◽  
Neuroendocrine Differentiation

scholarly journals Overexpression of an α1H(Cav3.2) T-type Calcium Channel during Neuroendocrine Differentiation of Human Prostate Cancer Cells

2002 ◽  
Vol 277 (13) ◽  
pp. 10824-10833 ◽  
Author(s):  
Pascal Mariot ◽  
Karine Vanoverberghe ◽  
Nathalie Lalevée ◽  
Michel F. Rossier ◽  
Natalia Prevarskaya
Keyword(s):  
Prostate Cancer ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Neuroendocrine Differentiation ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells

scholarly journals Erratum: Corrigendum: Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Xue-Long Wang ◽  
Bin Tian ◽  
Ya Huang ◽  
Xiao-Yan Peng ◽  
Li-Hua Chen ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Calcium Channel

Involvement of Src kinase in T-type calcium channel-dependent neuronal differentiation of NG108-15 cells by hydrogen sulfide

2010 ◽  
Vol 114 (2) ◽  
pp. 512-519 ◽  
Author(s):  
Takeshi Tarui ◽  
Kazuki Fukami ◽  
Keita Nagasawa ◽  
Shigeru Yoshida ◽  
Fumiko Sekiguchi ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Calcium Channel ◽  
Neuronal Differentiation ◽  
Src Kinase ◽  
Channel Dependent

Endogenous and exogenous hydrogen sulfide facilitates T-type calcium channel currents in Cav3.2-expressing HEK293 cells

2014 ◽  
Vol 445 (1) ◽  
pp. 225-229 ◽  
Author(s):  
Fumiko Sekiguchi ◽  
Yosuke Miyamoto ◽  
Daiki Kanaoka ◽  
Hiroki Ide ◽  
Shigeru Yoshida ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Calcium Channel ◽  
Hek293 Cells ◽  
Channel Currents

scholarly journals Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Xue-Long Wang ◽  
Bin Tian ◽  
Ya Huang ◽  
Xiao-Yan Peng ◽  
Li-Hua Chen ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Hydrogen Sulfide ◽  
Calcium Channel ◽  
Intradermal Injection ◽  
Independent Manner ◽  
C Fibers ◽  
Itch Sensation ◽  
Μ Opioid Receptor ◽  
Pharmacological Blockade ◽  
Endogenous Precursor

Abstract The contributions of gasotransmitters to itch sensation are largely unknown. In this study, we aimed to investigate the roles of hydrogen sulfide (H2S), a ubiquitous gasotransmitter, in itch signaling. We found that intradermal injection of H2S donors NaHS or Na2S, but not GYY4137 (a slow-releasing H2S donor), dose-dependently induced scratching behavior in a μ-opioid receptor-dependent and histamine-independent manner in mice. Interestingly, NaHS induced itch via unique mechanisms that involved capsaicin-insensitive A-fibers, but not TRPV1-expressing C-fibers that are traditionally considered for mediating itch, revealed by depletion of TRPV1-expressing C-fibers by systemic resiniferatoxin treatment. Moreover, local application of capsaizapine (TRPV1 blocker) or HC-030031 (TRPA1 blocker) had no effects on NaHS-evoked scratching. Strikingly, pharmacological blockade and silencing of Cav3.2 T-type calcium channel by mibefradil, ascorbic acid, zinc chloride or Cav3.2 siRNA dramatically decreased NaHS-evoked scratching. NaHS induced robust alloknesis (touch-evoked itch), which was inhibited by T-type calcium channels blocker mibefradil. Compound 48/80-induced itch was enhanced by an endogenous precursor of H2S (L-cysteine) but attenuated by inhibitors of H2S-producing enzymes cystathionine γ-lyase and cystathionine β-synthase. These results indicated that H2S, as a novel nonhistaminergic itch mediator, may activates Cav3.2 T-type calcium channel, probably located at A-fibers, to induce scratching and alloknesis in mice.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

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