Involvement of ERK in NMDA receptor-independent cortical neurotoxicity of hydrogen sulfide

2011 ◽  
Vol 414 (4) ◽  
pp. 727-732 ◽  
Author(s):  
Yuko Kurokawa ◽  
Fumiko Sekiguchi ◽  
Satoko Kubo ◽  
Yoshiko Yamasaki ◽  
Sachi Matsuda ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Nmda Receptor

P47 A novel hydrogen sulfide-releasing NMDA receptor antagonist prevents ischemic neuronal death

Nitric Oxide ◽  
2012 ◽  
Vol 27 ◽  
pp. S33 ◽  
Author(s):  
Eizo Marutani ◽  
Shizuko Kosugi ◽  
Kentaro Tokuda ◽  
Ashok Khatri ◽  
Rebecca Nguyen ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Neuronal Death ◽  
Nmda Receptor Antagonist

scholarly journals Hydrogen Sulfide’s Involvement in Modulating Nociception

2009 ◽  
Vol 5;12 (5;9) ◽  
pp. 901-910
Author(s):  
Howard Smith
Keyword(s):  
Hydrogen Sulfide ◽  
Ion Channels ◽  
Nmda Receptor ◽  
Calcium Channels ◽  
Molecular Mechanisms ◽  
Katp Channels ◽  
Long Term Potentiation ◽  
Primary Role ◽  
Key Words Pain ◽  
Nmda Receptor Complex

Hydrogen sulfide (H2S) is a malodorous gas which functions as an endogenous gasotransmitter in humans. It is becoming appreciated that H2S may be involved in a wide variety of processes including nociceptive processes. The molecular mechanisms responsible for many of the activities of H2S remain uncertain, however, H2S increases cAMP levels in neuronal and glial cell lines and primary neuron cultures with hyperpolarization. H2S may be involved in multiple signaling pathways and produce various effects on ion channels (e.g. T-type calcium channel currents, ATP-sensitive K+ (KATP) channels) which may inhibit or promote nociception. It is also conceivable that H2S may affect the n-methyl-d aspartate (NMDA) receptor complex and/or TRPA1 ion channels which may modulate nociceptive processes. It appears that H2S may regulate key neuronal functions, including the induction of hippocampal long-term potentiation, a synaptic model of learning and memory thought to involve the NMDA receptor as well as the release of corticotrophinreleasing hormone from the hypothalamus. It seems that the primary role of H2S in nociceptive processes is the activation of T-type calcium channels leading to facilitation of pronociceptive processes. A secondary contribution to the facilitation of pronociceptive processes may come from H2S-induced activation. It would appear that much like other gasotransmitters (e.g. nitric oxide), endogenous H2S may be involved in multiple physiologic processes and its effects remain complex, difficult to predict, and may vary depending on the specific environment/circumstances/location where it is generated. A greater understanding of the clinically significant human physiology of H2S and hydrogen sulfide’s effects on modulating nociceptive processes may potentially lead to novel targets for improving analgesia. Key words: Pain, nociception, hydrogen sulfide, calcium channels, analgesia, potassium channels

Regulation of emotional memory by hydrogen sulfide: role of GluN2B-containing NMDA receptor in the amygdala

2014 ◽  
Vol 132 (1) ◽  
pp. 124-134 ◽  
Author(s):  
Can-Ming Wang ◽  
Yuan-Jian Yang ◽  
Jie-Ting Zhang ◽  
Jue Liu ◽  
Xin-Lei Guan ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Nmda Receptor ◽  
Emotional Memory

scholarly journals Hydrogen sulfide mitigates diabetic nephropathy through NMDA receptor mediated renal remodeling

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Sourav Kundu ◽  
Aaron Tyagi ◽  
Denise Coley ◽  
Pushpakumar Sathnur ◽  
Utpal Sen
Keyword(s):  
Diabetic Nephropathy ◽  
Hydrogen Sulfide ◽  
Nmda Receptor

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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