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

Kurokawa, Y; Sekiguchi, Fumiko; Kubo, Satoko; Yamasaki, Yoshiko; Matsuda, Sachi; Okamoto, Yoh; Sekimoto, Teruki; Fukatsu, Anna; Nishikawa, Hiroyuki; Kume, Toshiaki; Fukushima, Nobuyuki; Akaike, Akinori; Kawabata, Atsufumi

doi:10.1016/j.bbrc.2011.09.144

Cited by 24 publications

(15 citation statements)

References 30 publications

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“…For example, the treatment of mouse cardiomyocytes with H 2 S donor (NaHS) induces ERK phosphorylation, while inhibition of the endogenous production of the gas has an opposite effect [41]. The identical treatment conditions for the mouse embryonal cortical neuron culture led to similar results [42]. Moreover, the authors use different inhibitors to show that the NaHS regulation of ERK phosphorylation depends on the MEK1 activity.…”

Section: Regulation Of the Ras-erk Signaling-dependent Dnmts Transcrimentioning

confidence: 61%

“…There is a growing number of studies on the role of protein sulfhydration in the cell signaling [7]. Some of them are dedicated to the Ras-ERK signaling dependence on the sulfhydration, the level of H 2 S concentration and the activity of H 2 S producing enzymes [41][42][43]. It is well-known that the ERK proteins dissociate from binding partner MEK and undergo activation-based phosphorylation to perform their function [35].…”

Section: Regulation Of the Ras-erk Signaling-dependent Dnmts Transcrimentioning

confidence: 99%

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A potential role of hydrogen sulfide (H2S) in the regulation of the Ras-ERK signaling-dependent transcription of DNA methyltransferases

Nikitina

2016

Biopolym. Cell

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The Ras-ERK cell signaling regulates transcription of DNA methyl-transferases (DNMTs). A role of H 2 S in regulation of the Ras-ERK signaling activity and DNMTs expression has also been shown. Here we propose a hypothesis that H 2 S regulates the Ras-ERK signaling-dependent DNMTs transcription. Oxidative stress, lipid metabolism, protein sulfhydration, nitrosylation and nitration are the main targets of regulation by H 2 S. These cell processes are important for the post-translational modifications (PTMs) of the Ras-ERK signaling pathway enzymes. We provide evidence for the dependence of DNMTs transcription on the PTMs of the enzymes of the Ras-ERK signaling pathway regulated by H 2 S.

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Section: Regulation Of the Ras-erk Signaling-dependent Dnmts Transcrimentioning

confidence: 61%

Section: Regulation Of the Ras-erk Signaling-dependent Dnmts Transcrimentioning

confidence: 99%

A potential role of hydrogen sulfide (H2S) in the regulation of the Ras-ERK signaling-dependent transcription of DNA methyltransferases

Nikitina

2016

Biopolym. Cell

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“…Depending upon the type of neuron and its metabolic state, activation of ERKs can either be neuroprotective (Franceschini et al, 206; Dagda et al, 2008) or can promote cell death (He and Aizenman, 2010; Kurokawa et al, 2011). Studies of hippocampal neurons have shown that ERK activation mediates mitochondrial biogenesis in response to BDNF which, in turn, promotes synapse formation and maintenance (Cheng et al, 2012).…”

Section: Signaling Pathways Shared By Hormetic Phytochemicals and mentioning

confidence: 99%

Neurohormetic phytochemicals: An evolutionary–bioenergetic perspective

Murugaiyah

Mattson

2015

Neurochemistry International

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The impact of dietary factors on brain health and vulnerability to disease is increasingly appreciated. The results of epidemiological studies, and intervention trials in animal models suggest that diets rich in phytochemicals can enhance neuroplasticity and resistance to neurodegeneration. Here we describe how interactions of plants and animals during their co-evolution, and resulting reciprocal adaptations, have shaped the remarkable characteristics of phytochemicals and their effects on the physiology of animal cells in general, and neurons in particular. Survival advantages were conferred upon plants capable of producing noxious bitter-tasting chemicals, and on animals able to tolerate the phytochemicals and consume the plants as an energy source. The remarkably diverse array of phytochemicals present in modern fruits, vegetables spices, tea and coffee may have arisen, in part, from the acquisition of adaptive cellular stress responses and detoxification enzymes in animals that enabled them to consume plants containing potentially toxic chemicals. Interestingly, some of the same adaptive stress response mechanisms that protect neurons against noxious phytochemicals are also activated by dietary energy restriction and vigorous physical exertion, two environmental challenges that shaped brain evolution. In this perspective article, we describe some of the signaling pathways relevant to cellular energy metabolism that are modulated by ‘neurohormetic phytochemicals’ (potentially toxic chemicals produced by plants that have beneficial effects on animals when consumed in moderate amounts). We highlight the cellular bioenergetics-related sirtuin, adenosine monophosphate activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) and insulin-like growth factor 1 (IGF-1) pathways. The inclusion of dietary neurohormetic phytochemicals in an overall program for brain health that also includes exercise and energy restriction may find applications in the prevention and treatment of a range of neurological disorders.

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“…H 2 S appears to play dual or complex roles in many tissues/organs. In the nervous system, there is evidence not only for the neurotoxicity of H 2 S through activation of glutamate receptors including NMDA receptors (Cheung et al 2007) and activation of the MEK/ERK pathway (Kurokawa et al 2011) but also for the neuroprotection by H 2 S via multiple mechanisms such as activation of ATP-sensitive K + (K ATP ) and Cl À channels and elevation of intracellular glutathione levels (Kimura and Kimura 2004;Kimura et al 2006). Endogenous H 2 S is also involved in neuronal excitation via the Ca 2+ /calmodulinmediated pathway (Eto et al 2002) and modification of long-term potentiation (Abe and Kimura 1996) via enhancement of the cAMP-induced NMDA receptor response (Kimura 2000).…”

Section: Introductionmentioning

confidence: 99%

H2S and Pain: A Novel Aspect for Processing of Somatic, Visceral and Neuropathic Pain Signals

Terada

Kawabata

2015

Handbook of Experimental Pharmacology

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Hydrogen sulfide (H2S) formed by multiple enzymes including cystathionine-γ-lyase (CSE) targets Cav3.2 T-type Ca2+ channels (T-channels) and transient receptor potential ankyrin-1 (TRPA1). Intraplantar and intracolonic administration of H2S donors promotes somatic and visceral pain, respectively, via activation of Cav3.2 and TRPA1 in rats and/or mice. Injection of H2S donors into the plantar tissues, pancreatic duct, colonic lumen, or bladder causes T-channel-dependent excitation of nociceptors, determined as phosphorylation of ERK or expression of Fos in the spinal dorsal horn. Electrophysiological studies demonstrate that exogenous and/or endogenous H2S facilitates membrane currents through T-channels in NG108-15 cells and isolated mouse dorsal root ganglion (DRG) neurons that abundantly express Cav3.2 and also in Cav3.2-transfected HEK293 cells. In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder. In rats with neuropathy induced by L5 spinal nerve cutting or by repeated administration of paclitaxel, an anticancer drug, the neuropathic hyperalgesia is reversed by inhibitors of CSE or T-channels and by silencing of Cav3.2. Upregulation of Cav3.2 protein in DRG is detectable in the former, but not in the latter, neuropathic pain models. Thus, H2S appears to function as a nociceptive messenger by facilitating functions of Cav3.2 and TRPA1, and the enhanced function of the CSE/H2S/Cav3.2 pathway is considered to be involved in the pancreatitis- and cystitis-related pain and in neuropathic pain.

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

Cited by 24 publications

References 30 publications

A potential role of hydrogen sulfide (H2S) in the regulation of the Ras-ERK signaling-dependent transcription of DNA methyltransferases

A potential role of hydrogen sulfide (H2S) in the regulation of the Ras-ERK signaling-dependent transcription of DNA methyltransferases

Neurohormetic phytochemicals: An evolutionary–bioenergetic perspective

H2S and Pain: A Novel Aspect for Processing of Somatic, Visceral and Neuropathic Pain Signals

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