Hydrogen Sulfide Inhibits the Development of Atherosclerosis with Suppressing CX3CR1 and CX3CL1 Expression

Zhang, Huili; Guo, Changfa; Wu, Duojiao; Zhang, Alian; Gu, Tao; Wang, Liansheng; Wang, Changqian

doi:10.1371/journal.pone.0041147

Cited by 64 publications

(61 citation statements)

References 38 publications

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“…In this latter work, the rate of development of atherosclerosis in these animals could be reduced by replacement therapy with NaHS. The current consensus is therefore that lack of H 2 S contributes to accelerated progression of atherosclerosis (Szab o et al 2011;Xu et al 2014a;Zhang et al 2012). …”

Section: 2mentioning

confidence: 99%

H2S Synthesizing Enzymes: Biochemistry and Molecular Aspects

Huang

Moore

2015

Handbook of Experimental Pharmacology

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Hydrogen sulfide (H2S) is a biologically active gas that is synthesized naturally by three enzymes, cystathionine γ-lyase (CSE), cystathionine β-synthetase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). These enzymes are constitutively present in a wide array of biological cells and tissues and their expression can be induced by a number of disease states. It is becoming increasingly clear that H2S is an important mediator of a wide range of cell functions in health and in disease. This review therefore provides an overview of the biochemical and molecular regulation of H2S synthesizing enzymes both in physiological conditions and their modulation in disease states with particular focus on their regulation in asthma, atherosclerosis and diabetes. The importance of small molecule inhibitors in the study of molecular pathways, the current use of common H2S synthesizing enzyme inhibitors and the relevant characteristics of mice in which these enzymes have been genetically deleted will also be summarized. With a greater understanding of the molecular regulation of these enzymes in disease states, as well as the availability of novel small molecules with high specificity targeted towards H2S producing enzymes, the potential to regulate the biological functions of this intriguing gas H2S for therapeutic effect can perhaps be brought one step closer.

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Section: 2mentioning

confidence: 99%

H2S Synthesizing Enzymes: Biochemistry and Molecular Aspects

Huang

Moore

2015

Handbook of Experimental Pharmacology

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“…NaHS (100 µmol/L for 12 hrs) inhibited ICAM-1 expression in TNF-alpha-induced HUVECs via the NF-kB pathway [159]. Moreover, NaHS administration concentration-dependently (50-200 µM) reduced CX3CR1 and CX3CL1 expression in mouse peritoneal macrophages as well as CX3CR1-mediated chemotaxis [160]. In fat-fed apoE-KO mice, NaHS (1 mg/kg, i.p., daily) attenuated, and PPG (10 mg/kg, i.p., daily) exacerbated, the extent of atherosclerotic plaques [160].…”

Section: The Roles Of H 2 S and No In Atherosclerosismentioning

confidence: 99%

“…Moreover, NaHS administration concentration-dependently (50-200 µM) reduced CX3CR1 and CX3CL1 expression in mouse peritoneal macrophages as well as CX3CR1-mediated chemotaxis [160]. In fat-fed apoE-KO mice, NaHS (1 mg/kg, i.p., daily) attenuated, and PPG (10 mg/kg, i.p., daily) exacerbated, the extent of atherosclerotic plaques [160]. H 2 S (50 µM) attenuated H 2 O 2 and oxidized LDL (oxLDL)-mediated endothelial cytotoxicity in HUVECs [161].…”

Section: The Roles Of H 2 S and No In Atherosclerosismentioning

confidence: 99%

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Altaany¹,

Moccia²,

Munaron³

et al. 2014

CMC

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The endothelium is a cellular monolayer that lines the inner surface of blood vessels and plays a central role in the maintenance of cardiovascular homeostasis by controlling platelet aggregation, vascular tone, blood fluidity and fibrinolysis, adhesion and transmigration of inflammatory cells, and angiogenesis. Endothelial dysfunctions are associated with various cardiovascular diseases, including atherosclerosis, hypertension, myocardial infarction, and cardiovascular complications of diabetes. Numerous studies have established the antiinflammatory, anti-apoptotic, and anti-oxidant effects of hydrogen sulfide (H 2 S), the latest member to join the gasotransmitter family along with nitric oxide and carbon monoxide, on vascular endothelium. In addition, H 2 S may prime endothelial cells (ECs) toward angiogenesis and contribute to wound healing, aside to its well-known ability to relax vascular smooth muscle cells (VSMCs), thereby reducing blood pressure. Finally, H 2 S may inhibit VSMC proliferation and platelet aggregation. Consistently, a deficit in H 2 S homeostasis is involved in the pathogenesis of atherosclerosis and of hyperglycaemic endothelial injury. Therefore, the application of H 2 S-releasing drugs or using gene therapy to increase endogenous H 2 S level may help restore endothelial function and antagonize the progression of cardiovascular diseases. The present article reviews recent studies on the role of H 2 S in endothelial homeostasis, under both physiological and pathological conditions, and its putative therapeutic applications. Endothelial structure and functionThe endothelium lines the luminal surface of the entire vascular tree and the cardiac chambers, where it is termed endocardium. As a consequence, the endothelium presents a rather broad extension (300 to 1000 m 2 ) and weight (1.5 kg), achieving sizes comparable to other vital organs of the human body [1,2]. The endothelium can, therefore, be regarded as a real "organ spread across the organism" [3] and, as such, not only it is important for the regulation of local tissue functions, but also for maintaining the whole organism homeostasis [4]. Vascular endothelial cells (ECs) possess a polarized architecture: their luminal membrane is directly exposed to hematic constituents and circulating cells, while the basolateral surface is separated from surrounding tissues by a glycoprotein basement membrane -the sub-endothelial basement -which is formed by fibronectin, laminin, and collagen and is secreted by ECs themselves [2].Heterogeneity is, however, the hallmark of endothelium. ECs differ in morphology, function, and gene expression profile, so that even neighbouring cells from the same organ and blood vessel type exhibit distinct features [4]. For instance, vascular ECs may vary in size, shape, thickness and position of the nucleus. Albeit oriented along direction of blood flow, to attenuate the impact of shear stress forces on the vascular wall, microvascular ECs are rather thin (0.1 µm) and spindle-like, whilst their macrovascul...

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“…Besides, NaHS inhibited ICAM-1 expression induced by tumor necrosis factor (TNF)-α stimulation via hampering IκB degradation in HUVECs [113]. Furthermore, Wang et al [114] suggested that H 2 S inhibited progression of atherosclerosis in ApoE KO mice with high-fat diet via downregulating CX3CR1 and CX3CL1 expression on macrophages in the lesion plaque in vivo . In addition, exogenous NaHS achieved its beneficial effects on diabetes accelerated atherosclerosis by inducing KEAP1 sulfhydration and NRF2 activation [51].…”

Section: Evidence Related To Atherosclerosis Prevention and Treatmentmentioning

confidence: 99%

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

Zj¹,

Wu²,

Guo³

et al. 2017

Cell Physiol Biochem

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Hydrogen sulfide (H₂S) is now admitted as a third gasotransmitter together with nitric oxide (NO) and carbon monoxide (CO), albeit it was originally considered as a foul and poisonous gas. Endogenous H₂S production in mammalian cells is counting on the three enzymes acting on cysteine. Involvement of H₂S in various physiological and pathological processes has been extensively studied in the last fifteen years. Mounting evidence suggests that H₂S is able to protect against atherosclerosis development and progression. Exogenous H₂S supplement has salutary effects on atherogenesis, and reduction of the endogenous H₂S level accelerates atherosclerosis. The anti-atherosclerotic mechanisms of H₂S have been descried in different aspects, including endothelium preservation, antioxidative action, anti-inflammatory responses, vasorelaxation, regulation of ion channels, etc. However, further investigation is still needed to help us gain more insights into the fundamental underlying mechanisms, and that will allow us to design better therapeutic applications of H₂S in the treatment of atherosclerosis.

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Hydrogen Sulfide Inhibits the Development of Atherosclerosis with Suppressing CX3CR1 and CX3CL1 Expression

Cited by 64 publications

References 38 publications

H2S Synthesizing Enzymes: Biochemistry and Molecular Aspects

H2S Synthesizing Enzymes: Biochemistry and Molecular Aspects

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

Atherosclerosis and the Hydrogen Sulfide Signaling Pathway – Therapeutic Approaches to Disease Prevention

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