Effect of Hydrogen Sulfide on the Mitogen-Activated Protein Kinase Signaling Pathway in Cultured Skin Macrophages of Burned Rats

Li, Yi; Wang, Hongjin; Wang, Xian-Zhen; Li, Xing-Long; Zhang, Xin; Lv, Hong

doi:10.1016/j.jss.2019.07.092

Cited by 7 publications

(4 citation statements)

References 17 publications

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“…These sites can be a potential target for H 2 S interaction with them, which can modify their activity. It should be noted that H 2 S can modulate the activity of various protein kinases [50]. It is known that kinases MAP JNK, p38, ERK, etc.…”

Section: Discussionmentioning

confidence: 99%

The Role of Hydrogen Sulfide in the Localization and Expression of p53 and Cell Death in the Nervous Tissue in Traumatic Brain Injury and Axotomy

Rodkin,

Nwosu,

Raevskaya

et al. 2023

IJMS

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Traumatic brain injury (TBI) is one of the leading causes of disability and death worldwide. It is characterized by various molecular–cellular events, with the main ones being apoptosis and damage to axons. To date, there are no clinically effective neuroprotective drugs. In this study, we examined the role of hydrogen sulfide (H2S) in the localization and expression of the key pro-apoptotic protein p53, as well as cell death in the nervous tissue in TBI and axotomy. We used a fast donor (sodium sulphide, Na2S) H2S and a classic inhibitor (aminooxyacetic acid, AOAA) of cystathionine β-synthase (CBS), which is a key enzyme in H2S synthesis. These studies were carried out on three models of neurotrauma in vertebrates and invertebrates. As a result, it was found that Na2S exhibits a pronounced neuroprotective effect that reduces the number of TUNEL-positive neurons and glial cells in TBI and apoptotic glia in axotomy. This effect could be realized through the Na2S-dependent decrease in the level of p53 in the cells of the nervous tissue of vertebrates and invertebrates, which we observed in our study. We also observed the opposite effect when using AOAA, which indicates the important role of CBS in the regulation of p53 expression and death of neurons and glial cells in TBI and axotomy.

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Section: Discussionmentioning

confidence: 99%

The Role of Hydrogen Sulfide in the Localization and Expression of p53 and Cell Death in the Nervous Tissue in Traumatic Brain Injury and Axotomy

Rodkin,

Nwosu,

Raevskaya

et al. 2023

IJMS

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“…In a word, the present results indicated that the novel H 2 S donor not only reduced microglial pro-inflammatory profiles, but also simultaneously increased microglial anti-inflammatory profiles. Nowadays, exogenous H 2 S donors, in a variety of experimental systems, were found to induce the activation of signal transduction effects (such as p38, Akt, Erk, JNK, and Stat3), which in turn, produce different functional responses to the expression of various microglia surface antigens and secreted cytokines and exert anti-inflammatory effects ( Lee et al, 2010 , 2016 ; Sulen et al, 2016 ; Zhang et al, 2017 ; Cao et al, 2018 ; Li et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

A Novel Hydrogen Sulfide Donor Reduces Pilocarpine-Induced Status Epilepticus and Regulates Microglial Inflammatory Profile

Liu

Zhu

et al. 2021

Front. Cell. Neurosci.

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Although epilepsy is one of the most common neurologic disorders, there is still a lack of effective therapeutic drugs for it. Recently, we synthesized a novel hydrogen sulfide (H2S) donor, which is found to reduce seizures in animal models effectively. But it remains to be determined for its mechanism. In the present study, we found that the novel H2S donor could reduce pilocarpine-induced seizures in mice. It alleviated the epileptic behavior, the hippocampal electroencephalography (EEG) activity of seizures, and the damage of hippocampal neurons in status epilepticus mice. In addition, the novel H2S donor could reduce microglial inflammatory response. It not only reduced the upregulation of pro-inflammatory markers [inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2)] in status epilepticus mice, but also increased the levels of microglial anti-inflammatory marker arginase-1 (Arg-1). In lipopolysaccharide-treated microglia BV2 cells, administration of the H2S donor also significantly reduced the lipopolysaccharide-induced upregulation of the expression of the pro-inflammatory markers and increased the expression of the anti-inflammatory markers. Thus, the novel H2S donor regulates microglial inflammatory profile in status epilepticus mice and in vitro. These results suggested that the novel H2S donor can reduce seizures and regulate microglial inflammatory profile, which may be a novel mechanism and potential therapeutic strategy of the H2S donor anti-seizures.

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“…2). Inspirationally, previous studies have proved that H 2 S can regulate cell proliferation and survival in different cells, including endotheliocytes, cardiomyocytes, neurocytes, astrocytes, granulocytes, skin macrophages, and so on [14][15][16][17]. Additionally, the PI3K/AKT pathway, ATP-sensitive potassium channel (KATP)/MAPK pathway, protein kinase C, and nitric oxide synthase were reported to be involved in the pro-proliferation and cytoprotective effect of H 2 S. Further research studies are needed to discover the possible molecular mechanism of H 2 S in promoting melanocyte proliferation.…”

Section: Discussion/conclusionmentioning

confidence: 99%

Hydrogen Sulfide Promotes Cell Proliferation and Melanin Synthesis in Primary Human Epidermal Melanocytes

Ying

Wang

Jiang

et al. 2020

Skin Pharmacol Physiol

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Background/Aim: Hydrogen sulfide (H 2 S) has been found to act as a physiological intercellular messenger to regulate cell survival. In this study, we evaluated whether H 2 S could promote cell proliferation and melanin synthesis in human epidermal melanocytes (HEMs). Methods: Primary HEMs were cocultured with sodium hydrosulfide (NaHS, the most widely used H 2 S donor) or endogenously overexpressed with cystathionine-γ-lyase (CSE) gene, which is the most predominant H 2 S-producing enzyme. Then, cell viability, intracellular melanin content, tyrosinase (TYR) activity, and expression of microphthalmia-associated transcription factor (MITF), TYR, together with TYR-related protein 1 (TRP-1) in both transcript and protein levels, were detected. Results: We first confirmed that NaHS (10-100 μm) increased cell viability, intracellular melanin content, and TYR activity in a dose-dependent manner. Then, we found that endogenous H 2 S production also promoted cell proliferation, intracellular melanin content, and TYR activity. In addition, we observed the mRNA and protein expression of MITF, TYR, and TRP-1 was significantly up-regulated after NaHS treatment and CSE gene transfection. Conclusions: This study demonstrates that H 2 S promotes cell proliferation and melanin synthesis in HEMs, which indicates pharmacologic regulation of H 2 S may be potential treatment for skin disorders caused by loss of melanocytes or dysfunction of melanogenesis.

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Effect of Hydrogen Sulfide on the Mitogen-Activated Protein Kinase Signaling Pathway in Cultured Skin Macrophages of Burned Rats

Cited by 7 publications

References 17 publications

The Role of Hydrogen Sulfide in the Localization and Expression of p53 and Cell Death in the Nervous Tissue in Traumatic Brain Injury and Axotomy

The Role of Hydrogen Sulfide in the Localization and Expression of p53 and Cell Death in the Nervous Tissue in Traumatic Brain Injury and Axotomy

A Novel Hydrogen Sulfide Donor Reduces Pilocarpine-Induced Status Epilepticus and Regulates Microglial Inflammatory Profile

Hydrogen Sulfide Promotes Cell Proliferation and Melanin Synthesis in Primary Human Epidermal Melanocytes

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