Hydrogen sulfide is a novel mediator of lipopolysaccharide‐induced inflammation in the mouse

Li, Ling; Bhatia, Madhav; Zhu, Yi Zhun; Zhu, Yi; Ramnath, Raina Devi; Wang, Zhong Jing; Anuar, Farhana; Whiteman, Matthew; Salto-Tellez, Manuel; Moore, Philip K.

doi:10.1096/fj.04-3583fje

Cited by 722 publications

(555 citation statements)

References 33 publications

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“…H 2 S equilibrates with aqueous sulphides (HS À and S 2 À ) in biological environments and has vital roles in various physiological and pathological processes, including vasorelaxation 5 , angiogenesis 6 , cerebral microcirculation 7 , neurotransmission 8,9 , inflammation 10 , apoptosis 11 , insulin signalling inhibition 12 , oxygen sensing 13 and energy production in mitochondria 14 . Meanwhile, the H 2 S levels are related to a number of diseases, such as Down syndrome 15 , Alzheimer disease 16 , hyperglycaemia 17 , ischaemia 18 and so on.…”

Section: Doi: 101038/ncomms2722mentioning

confidence: 99%

Highly sensitive sulphide mapping in live cells by kinetic spectral analysis of single Au-Ag core-shell nanoparticles

et al. 2013

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Hydrogen sulphide (H 2 S) is a gaseous signalling agent that has important regulatory roles in many biological systems but remains difficult to measure in living biological specimens. Here we introduce a new method for highly sensitive sulphide mapping in live cells via singleparticle plasmonic spectral imaging that uses Au-Ag core-shell nanoparticles as probes. This strategy is based on Ag 2 S formation-induced spectral shifts of the nanoprobes, which is not only highly selective towards sulphide but also shows a linear logarithmic dependence on sulphide concentrations from 0.01 nM to 10 mM. A theoretical model was established that successfully explained the experimental observations, suggesting that the local sulphide concentration as well as its oscillations can be determined indirectly from kinetic measurements of the spectral shifts of the nanoprobes. We demonstrated for the first time the realtime mapping of local variations of sulphide levels in live cells with nM sensitivity.

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Section: Doi: 101038/ncomms2722mentioning

confidence: 99%

Highly sensitive sulphide mapping in live cells by kinetic spectral analysis of single Au-Ag core-shell nanoparticles

et al. 2013

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“…H 2 S was administered in the form of NaHS (Sigma, St. Louis, Missouri, USA), which has been well established as a reliable donor of H 2 S (Abe and Kimura 1996;Zhao et al 2001;Deplancke and Gaskins 2003;Li et al 2005). When NaHS is dissolved in saline, about one-third of H 2 S exists as undissociated gas, and the remaining two-thirds is HS − .…”

Section: Chemicalsmentioning

confidence: 99%

Hydrogen Sulfide, a Gaseous Transmitter, Stimulates Proliferation of Interstitial Cells of Cajal via Phosphorylation of AKT Protein Kinase

Huang

Tong

et al. 2010

Tohoku J. Exp. Med.

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“…In an in vivo model for myocardial ischemia-reperfusion, a U-shaped H 2 S dose dependence curve was observed, with the cardioprotective effect of H 2 S decreasing at higher concentrations (7). In a rat model of stroke, administration of high NaHS levels increased infarct volume (42), and H 2 S was found to be proinflammatory in a mouse endotoxic shock model (8). Mutations in CBS are the most common cause of severe hyperhomocysteinemia in comparison with defects elsewhere in the pathway (e.g.…”

mentioning

confidence: 95%

H2S Biogenesis by Human Cystathionine γ-Lyase Leads to the Novel Sulfur Metabolites Lanthionine and Homolanthionine and Is Responsive to the Grade of Hyperhomocysteinemia

Chiku

Padovani

Zhu

et al. 2009

Journal of Biological Chemistry

434

424

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Although there is a growing recognition of the significance of hydrogen sulfide (H 2 S) as a biological signaling molecule involved in vascular and nervous system functions, its biogenesis and regulation are poorly understood. It is widely assumed that desulfhydration of cysteine is the major source of H 2 S in mammals and is catalyzed by the transsulfuration pathway enzymes, cystathionine ␤-synthase and cystathionine ␥-lyase (CSE). In this study, we demonstrate that the profligacy of human CSE results in a variety of reactions that generate H 2 S from cysteine and homocysteine. The ␥-replacement reaction, which condenses two molecules of homocysteine, yields H 2 S and a novel biomarker, homolanthionine, which has been reported in urine of homocystinuric patients, whereas a ␤-replacement reaction, which condenses two molecules of cysteine, generates lanthionine. Kinetic simulations at physiologically relevant concentrations of cysteine and homocysteine, reveal that the ␣,␤-elimination of cysteine accounts for ϳ70% of H 2 S generation. However, the relative importance of homocysteinederived H 2 S increases progressively with the grade of hyperhomocysteinemia, and under conditions of severely elevated homocysteine (200 M), the ␣,␥-elimination and ␥-replacement reactions of homocysteine together are predicted to account for ϳ90% of H 2 S generation by CSE. Excessive H 2 S production in hyperhomocysteinemia may contribute to the associated cardiovascular pathology.H 2 S is the newest member of a growing list of gaseous signaling molecules that modulate physiological functions (1-3). Concentrations of H 2 S ranging from 50 to 160 M have been reported in the brain (4), where it appears to function as a neuromodulator by potentiating the activity of the N-methyl-Daspartate receptor and by altering induction of long term potentiation in the hippocampus, important for memory and learning (5). H 2 S levels in human plasma are reported to be ϳ50 M, and in vitro studies suggest that it functions as a vasodilator by opening K ATP channels in vascular smooth muscle cells (6).A recent in vivo study has demonstrated the efficacy of H 2 S in attenuating myocardial ischemia-reperfusion injury by protecting mitochondrial function (7). The role of H 2 S in inflammation is suggested by several studies (8 -11); however, the underlying mechanism is unknown. Remarkably, H 2 S can also induce a state of suspended animation in mice by decreasing the metabolic rate and the core body temperature presumably by inhibiting cytochrome c oxidase in the respiratory chain (12).Endogenous H 2 S is presumed to be generated primarily by desulfhydration of cysteine catalyzed by the two pyridoxal phosphate (PLP) 3 -dependent enzymes in the transsulfuration pathway: cystathionine ␤-synthase (CBS) and cystathionine ␥-lyase (CSE) (13,14). In fact, it is widely assumed, based on the reported absences of CSE in the brain (15) and of H 2 S in the brain of CBS knock-out mice (16), that CBS is the primary source of H 2 S in this organ, whereas CSE plays the...

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Hydrogen sulfide is a novel mediator of lipopolysaccharide‐induced inflammation in the mouse

Cited by 722 publications

References 33 publications

Highly sensitive sulphide mapping in live cells by kinetic spectral analysis of single Au-Ag core-shell nanoparticles

Highly sensitive sulphide mapping in live cells by kinetic spectral analysis of single Au-Ag core-shell nanoparticles

Hydrogen Sulfide, a Gaseous Transmitter, Stimulates Proliferation of Interstitial Cells of Cajal via Phosphorylation of AKT Protein Kinase

H2S Biogenesis by Human Cystathionine γ-Lyase Leads to the Novel Sulfur Metabolites Lanthionine and Homolanthionine and Is Responsive to the Grade of Hyperhomocysteinemia

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