Pro‐apoptotic effect of endogenous H<sub>2</sub>S on human aorta smooth muscle cells

Yang, Guangdong; Wu, Lingyun; Wang, Rui

doi:10.1096/fj.05-4712fje

Cited by 290 publications

(205 citation statements)

References 38 publications

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“…The accumulation of evidence that mitochondrial function and structure was preserved after myocardial infarction in mice treated with H 2 S was further corroborated by the decreased activation of caspase-3 and a decrease in the number of TUNEL positive nuclei, suggesting that H 2 S was capable of inhibiting the progression of apoptosis after MI-R injury. The capacity of H 2 S to modulate apoptosis has been controversial with some groups reporting H 2 S mediating apoptosis (28)(29)(30) and others citing inhibition (31,32). However, it is important to note that none of the studies to date have used in vivo model systems and have used varying concentrations of H 2 S, some well outside the physiologically relevant range.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Elrod¹,

Calvert²,

Morrison

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

1,029

892

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The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemiareperfusion (MI-R). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H2S by cardiac-specific overexpression of cystathionine ␥-lyase (␣-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.

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Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Elrod¹,

Calvert²,

Morrison

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

1,029

892

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“…Among other functionally relevant Cys modifications are (i) a thioether bond with farnesyl or geranylgeranyl groups (leading to protein lipidation, and finally to membrane anchoring, 103), and (ii) mixed disulfide bonds with endogenous hydrogen sulfide (H 2 S). The latter modification has been linked to various physiological (22,46,100,101,102) and structural effects (45), revealing H 2 S as a potent signal molecule, and Cys as its amino acid target. …”

Section: Regulatory Cysmentioning

confidence: 99%

Redox Biology: Computational Approaches to the Investigation of Functional Cysteine Residues

Marino

Gladyshev

2011

Antioxidants & Redox Signaling

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Cysteine (Cys) residues serve many functions, such as catalysis, stabilization of protein structure through disulfides, metal binding, and regulation of protein function. Cys residues are also subject to numerous post-translational modifications. In recent years, various computational tools aiming at classifying and predicting different functional categories of Cys have been developed, particularly for structural and catalytic Cys. On the other hand, given complexity of the subject, bioinformatics approaches have been less successful for the investigation of regulatory Cys sites. In this review, we introduce different functional categories of Cys residues. For each category, an overview of state-of-the-art bioinformatics methods and tools is provided, along with examples of successful applications and potential limitations associated with each approach. Finally, we discuss Cys-based redox switches, which modify the view of distinct functional categories of Cys in proteins. Antioxid. Redox Signal. 15, 135-146.

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“…The anti-apoptotic action of H 2 S is related to its capability to prevent the mitochondrial membrane potential dissipation by the activation of multiple mechanism, but all through K ATP channels [15]. On the other hand, H 2 S stimulates VSMC apoptosis [114]. The increased endogenous production of H 2 S derived from CSE overexpression induces apoptosis in human VSMCs by activating ERK1/2 and capsase-3 [114].…”

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

confidence: 99%

“…On the other hand, H 2 S stimulates VSMC apoptosis [114]. The increased endogenous production of H 2 S derived from CSE overexpression induces apoptosis in human VSMCs by activating ERK1/2 and capsase-3 [114]. Interestingly, VSMCs isolated from CSE-KO mice were more susceptible to apoptosis induced by exogenous H 2 S at 100 µM.…”

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

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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Pro‐apoptotic effect of endogenous H₂S on human aorta smooth muscle cells

Cited by 290 publications

References 38 publications

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Redox Biology: Computational Approaches to the Investigation of Functional Cysteine Residues

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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Pro‐apoptotic effect of endogenous H2S on human aorta smooth muscle cells

Cited by 290 publications

References 38 publications

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

Redox Biology: Computational Approaches to the Investigation of Functional Cysteine Residues

Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide

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Pro‐apoptotic effect of endogenous H₂S on human aorta smooth muscle cells