Intravital Microscopic Methods to Evaluate Anti-inflammatory Effects and Signaling Mechanisms Evoked by Hydrogen Sulfide

Zuidema, Mozow Y.; Korthuis, Ronald J.

doi:10.1016/bs.mie.2014.11.022

Cited by 14 publications

(23 citation statements)

References 72 publications

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“…Using intravital microscopy, H 2 S donors are found to attenuate the leukocyte adherence in rat mesenteric arteries induced by aspirin, this effect may be likely dependent on activation of KATP channels (Zanardo et al, 2006;Zuidema and Korthuis, 2015). In accordance with this, blockade of endogenous H 2 S exacerbates leukocyte-mediated inflammation in the endothelium (Zanardo et al, 2006).…”

Section: Role Of H 2 S In Endothelial Inflammationmentioning

confidence: 65%

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

et al. 2020

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Endothelial cells are important constituents of blood vessels that play critical roles in cardiovascular homeostasis by regulating blood fluidity and fibrinolysis, vascular tone, angiogenesis, monocyte/leukocyte adhesion, and platelet aggregation. The normal vascular endothelium is taken as a gatekeeper of cardiovascular health, whereas abnormality of vascular endothelium is a major contributor to a plethora of cardiovascular ailments, such as atherosclerosis, aging, hypertension, obesity, and diabetes. Endothelial dysfunction is characterized by imbalanced vasodilation and vasoconstriction, elevated reactive oxygen species (ROS), and proinflammatory factors, as well as deficiency of nitric oxide (NO) bioavailability. The occurrence of endothelial dysfunction disrupts the endothelial barrier permeability that is a part of inflammatory response in the development of cardiovascular diseases. As such, abrogation of endothelial cell activation/inflammation is of clinical relevance. Recently, hydrogen sulfide (H 2 S), an entry as a gasotransmitter, exerts diverse biological effects through acting on various targeted signaling pathways. Within the cardiovascular system, the formation of H 2 S is detected in smooth muscle cells, vascular endothelial cells, and cardiomyocytes. Disrupted H 2 S bioavailability is postulated to be a new indicator for endothelial cell inflammation and its associated endothelial dysfunction. In this review, we will summarize recent advances about the roles of H 2 S in endothelial cell homeostasis, especially under pathological conditions, and discuss its putative therapeutic applications in endothelial inflammation-associated cardiovascular disorders.

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Section: Role Of H 2 S In Endothelial Inflammationmentioning

confidence: 65%

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

et al. 2020

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“…Upon chemoattractant signalling in the lung, neutrophils first pass the endothelial barrier and migrate to the site of inflammation 5 , 21 . As it has been demonstrated in a model of small intestine ischemia-reperfusion injury, H 2 S can prevent leukocyte adhesion and rolling 16 – 18 . To address our above mentioned hypothesis, we established an in vitro neutrophil transmigration model using an endothelial monolayer (HUVEC cells) on a perforated insert (Fig.…”

Section: Discussionmentioning

confidence: 77%

“…Adding GYY4137 to the top medium completely inhibited this process. Our observations can be explained in several ways: First, the permeability of the endothelial barrier increased upon MIP-2 stimulation and decreased in response to H 2 S supplementation 18 , 43 , 44 , consequently reducing the capability of neutrophils to cross intercellular gaps. Second, H 2 S limits the pro-inflammatory signalling in stimulated HUVEC cells 34 , 45 , thus attracting fewer neutrophils.…”

Section: Discussionmentioning

confidence: 87%

“…In order to evaluate possible (pre)treatment options, we and others have previously shown that inhalation of hydrogen sulfide (H 2 S) prevents neutrophil accumulation in models of ventilator- 7 – 9 and lipopolysaccharide (LPS)-induced lung injury 10 – 14 . Although recent data suggest that H 2 S may limit neutrophil activation and transmigration by downregulating pulmonary expression of chemoattractant molecules 15 or by reducing leukocyte rolling and adhesion 15 – 18 , it remains completely unknown how H 2 S interacts with the neutrophilic inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

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Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury

Faller

Häusler

Goeft

et al. 2018

Sci Rep

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Transmigration and activation of neutrophils in the lung reflect key steps in the progression of acute lung injury (ALI). It is known that hydrogen sulfide (H2S) can limit neutrophil activation, but the respective mechanisms remain elusive. Here, we aimed to examine the underlying pathways in pulmonary inflammation. In vivo, C57BL/6N mice received the H2S slow releasing compound GYY4137 prior to lipopolysaccharide (LPS) inhalation. LPS challenge led to pulmonary injury, inflammation, and neutrophil transmigration that were inhibited in response to H2S pretreatment. Moreover, H2S reduced mRNA expression of macrophage inflammatory protein-2 (MIP-2) and its receptor in lung tissue, as well as the accumulation of MIP-2 and interleukin-1β in the alveolar space. In vitro, GYY4137 did not exert toxic effects on Hoxb8 neutrophils, but prevented their transmigration through an endothelial barrier in the presence and absence of MIP-2. In addition, the release of MIP-2 and reactive oxygen species from LPS-stimulated Hoxb8 neutrophils were directly inhibited by H2S. Taken together, we provide first evidence that H2S limits lung neutrophil sequestration upon LPS challenge. As proposed underlying mechanisms, H2S prevents neutrophil transmigration through the inflamed endothelium and directly inhibits pro-inflammatory as well as oxidative signalling in neutrophils. Subsequently, H2S pretreatment ameliorates LPS-induced ALI.

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“…Both are characterized by recruitment of neutrophils and other leukocytes to the affected tissue site, coincident with the production of cytokines, chemokines, and other proinflammatory stimuli that serve as directional cues (249, 310, 372, 446, 463). Leukocyte trafficking to ischemic sites occurs primarily during reperfusion and involves 11 distinct steps (594–596, 816a, 923a, see Fig. 10).…”

Section: Inflammation Plays a Prominent Role In The Reperfusion Compomentioning

confidence: 99%

Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

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626

565

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Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease.

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Intravital Microscopic Methods to Evaluate Anti-inflammatory Effects and Signaling Mechanisms Evoked by Hydrogen Sulfide

Cited by 14 publications

References 72 publications

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

Hydrogen sulfide limits neutrophil transmigration, inflammation, and oxidative burst in lipopolysaccharide-induced acute lung injury

Ischemia/Reperfusion

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