Hydrogen Sulfide, the Third Gaseous Signaling Molecule With Cardiovascular Properties, Is Decreased in Hemodialysis Patients

Perna, Alessandra F.; Luciano, Maria Grazia; Ingrosso, Diego; Raiola, Ilaria; Pulzella, Paola; Sepe, Immacolata; Lanza, Diana; Violetti, Eleonora; Capasso, Rosanna; Lombardi, Cinzia; Santo, Natale G. De

doi:10.1053/j.jrn.2010.05.004

Cited by 17 publications

(13 citation statements)

References 23 publications

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“…A causative role for HHcy in the development of cardiovascular and renal disease is the subject of ongoing debate [71,72]. However, several papers have reported that impaired conversion of Hcy into H2S and consequent H2S deficiency may, at least in part, be responsible for HHcy associated pathology [73][74][75].…”

Section: H2s In the Onset And Progression Of Renal Diseasementioning

confidence: 99%

Hydrogen sulfide in renal physiology, disease and transplantation – The smell of renal protection

et al. 2015

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Section: H2s In the Onset And Progression Of Renal Diseasementioning

confidence: 99%

Hydrogen sulfide in renal physiology, disease and transplantation – The smell of renal protection

et al. 2015

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“…It is also now generally accepted that it acts as a gaseous signalling transmitter along with carbon monoxide (CO) and nitric oxide (NO). Hydrogen sulfide is produced in vivo from L-cysteine predominately by cystathionine gamma-lyase (CSE), cystathionine beta synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) [1]. Expression of CSE in the periphery [2] and CBS in the central nervous system [3, 4] determines which enzyme is involved in hydrogen sulfide production at these sites.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Hydrogen Sulfide Production by Gene Silencing Attenuates Inflammatory Activity by Downregulation of NF-κB and MAP Kinase Activity in LPS-Activated RAW 264.7 Cells

Badiei

Muniraj

Chambers

et al. 2014

BioMed Research International

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Hydrogen sulfide is an endogenous inflammatory mediator produced by the activity of cystathionine γ-lyase (CSE) in macrophages. The objective of this study was to explore the mechanism by which hydrogen sulfide acts as an inflammatory mediator in lipopolysaccharide- (LPS-) induced macrophages. In this study, we used small interfering RNA (siRNA) to inhibit CSE expression in macrophages. We found that CSE silencing siRNA could reduce the LPS-induced activation of transcription factor nuclear factor-κB (NF-κB) significantly. Phosphorylation and activation of extra cellular signal-regulated kinase 1/2 (ERK1/2) increased in LPS-induced macrophages. We showed that phosphorylation of ERK in LPS-induced RAW 264.7 cells reached a peak 30 min after activation. Our findings show that silencing CSE gene by siRNA reduces phosphorylation and activation of ERK1/2 in LPS-induced RAW 264.7 cells. These findings suggest that siRNA reduces the inflammatory effects of hydrogen sulfide through the ERK-NF-κB signalling pathway and hydrogen sulfide plays its inflammatory role through ERK-NF-κB pathway in these cells.

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“…An observational study in coronary heart disease patients, hypertensives, and smokers, has also shown that plasma H 2 S is lower compared to normal subjects. Low H 2 S was found in hypertensive children as well [see [15] for review on this topic]. In this respect, it has recently been shown that H 2 S inhibits plasma renin activity by decreasing synthesis and release of renin in a rat model of renovascular hypertension [16].…”

Section: Biological Effectsmentioning

confidence: 99%

Hydrogen Sulfide, a Toxic Gas with Cardiovascular Properties in Uremia: How Harmful Is It?

Perna¹,

Lanza²,

Sepe³

et al. 2011

Blood Purif

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Hydrogen sulfide (H₂S) is a poisonous gas which can be lethal. However, it is also produced endogenously, thus belonging to the family of gasotransmitters along with nitric oxide and carbon monoxide. H₂S is in fact involved in mediating several signaling and cytoprotective functions, for example in the nervous, cardiovascular, and gastrointestinal systems, such as neuronal transmission, blood pressure regulation and insulin release, among others. When increased, it can mediate inflammation and apoptosis, with a role in shock. When decreased, it can be involved in atherosclerosis, hypertension, myocardial infarction, diabetes, sexual dysfunction, and gastric ulcer; it notably interacts with the other gaseous mediators. Cystathionine γ-lyase, cystathionine β-synthase, and 3-mercaptopyruvate sulfurtransferase are the principal enzymes involved in H₂S production. We have recently studied H₂S metabolism in the plasma of chronic hemodialysis patients and reported that its levels are significantly decreased. The plausible mechanism lies in the transcription inhibition of the cystathionine γ-lyase gene. The finding could be of importance considering that hypertension and high cardiovascular mortality are characteristic in these patients.

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Hydrogen Sulfide, the Third Gaseous Signaling Molecule With Cardiovascular Properties, Is Decreased in Hemodialysis Patients

Cited by 17 publications

References 23 publications

Hydrogen sulfide in renal physiology, disease and transplantation – The smell of renal protection

Hydrogen sulfide in renal physiology, disease and transplantation – The smell of renal protection

Inhibition of Hydrogen Sulfide Production by Gene Silencing Attenuates Inflammatory Activity by Downregulation of NF-κB and MAP Kinase Activity in LPS-Activated RAW 264.7 Cells

Hydrogen Sulfide, a Toxic Gas with Cardiovascular Properties in Uremia: How Harmful Is It?

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