Tumor Necrosis Factor Related Apoptosis Inducing Ligand (Trail) in Endothelial Response to Biomechanical and Biochemical Stresses in Arteries

D'Auria, Francesca; Centurione, Lucia; Centurione, MA; Angelini, Antonio; Pietro, Roberta Di

doi:10.1002/jcb.25223

Cited by 14 publications

(12 citation statements)

References 48 publications

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“…In the literature, a number of studies have shown that soluble TRAIL is able to induce the activation of some signal transduction pathways, promoting the survival of VSMCs and ECs. TRAIL also exerts a protective effect on the endothelium through its anti-inflammatory properties and the production of local nitric oxide (NO) [8]. Recently, there has been outstanding progress in the development of novel formulations to increase the circulatory half-life of TRAIL, thus improving the biological attributes of TRAIL-based therapies.…”

Section: The Opg/rankl/rank/trail System: Structures Localizationmentioning

confidence: 99%

The Role of Osteoprotegerin and Its Ligands in Vascular Function

Rochette

Méloux

Rigal

et al. 2019

IJMS

117

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The superfamily of tumor necrosis factor (TNF) receptors includes osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The OPG/RANKL/RANK system plays an active role in pathological angiogenesis and inflammation as well as cell survival. It has been demonstrated that there is crosstalk between endothelial cells and osteoblasts during osteogenesis, thus establishing a connection between angiogenesis and osteogenesis. This OPG/RANKL/RANK/TRAIL system acts on specific cell surface receptors, which are then able to transmit their signals to other intracellular components and modify gene expression. Cytokine production and activation of their receptors induce mechanisms to recruit monocytes and neutrophils as well as endothelial cells. Data support the role of an increased OPG/RANKL ratio as a possible marker of progression of endothelial dysfunction in metabolic disorders in relationship with inflammatory marker levels. We review the role of the OPG/RANKL/RANK triad in vascular function as well as molecular mechanisms related to the etiology of vascular diseases. The potential therapeutic strategies may be very promising in the future.

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Section: The Opg/rankl/rank/trail System: Structures Localizationmentioning

confidence: 99%

The Role of Osteoprotegerin and Its Ligands in Vascular Function

Rochette

Méloux

Rigal

et al. 2019

IJMS

117

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“…In particular, the TNF and TRAIL receptors become activated and initiate both death and pro-survival signaling. 26 By definition, our experimental model of HS produces a period of ischemia followed by a reperfusion event. Using this model, our laboratory has shown a direct correlation between apoptotic signaling and HS-induced vascular hyperpermeability.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Bcl-xL attenuates vascular hyperpermeability in a rat model of hemorrhagic shock

Tharakan

McNeal

Hunter

et al. 2015

Cell Death Discovery

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Following hemorrhagic shock (HS), vascular hyperpermeability i.e. the leakage of fluid, nutrients and proteins into the extravascular space occurs primarily due to the disruption of the endothelial cell-cell adherens junctional complex. Studies from our laboratory demonstrate that activation of the mitochondria mediated ‘intrinsic’ apoptotic signaling cascade has a significant role in modulating HS-induced hyperpermeability. Here we report the novel use of recombinant Bcl-xL, an anti-apoptotic protein, to control HS-induced vascular hyperpermeability. Our results corroborate involvement of vascular hyperpermeability and apoptotic signaling. Hemorrhagic shock (HS) (mean arterial pressure [MAP] was reduced to 40 mmHg for 60 minutes followed by resuscitation to 90 mmHg for 60 minutes) in rats resulted in vascular hyperpermeability as determined by intra-vital microscopy. Treatment of Bcl-xL (2.5ug/ml of rat blood in non-lipid cationic polymer, i.v.) before, during and even after HS attenuated or reversed HS-induced vascular hyperpermeability significantly (p<0.05). Conversely, treatment using Bcl-xL inhibitors, 2-methoxy antimycin (2-MeOAA) and ABT 737, significantly increased vascular hyperpermeability compared to sham (p<0.05). Bcl-xL treatment also decreased the amount of fluid volume required to maintain a MAP of 90 mmHg during resuscitation (p<0.05). HS resulted in increased mitochondrial ROS formation, reduction of ΔΨm, mitochondrial release of cytochrome c and significant activation of caspase-3 (p<0.05). All of these effects were significantly inhibited by Bcl-xL pre-treatment (p<0.05). Our results show that recombinant Bcl-xL is effective against HS-induced vascular hyperpermeability that appears to be mediated through preservation of ΔΨm and subsequent prevention of caspase-3 activation.

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“…In contrast to OPG, TRAIL is present in significantly lower plasma concentrations in people with CAD than in healthy people [6,34,[72][73][74][75]. It is the low plasma concentrations of TRAIL in this group of patients that are associated with a higher risk of CV mortality, a higher risk of post-infarction left ventricular remodelling and the development of HF [6,34,73,[76][77][78]. However, in patients with CAD, it is not only the plasma levels of TRAIL that are relevant.…”

Section: The Combination Of Opg and Trailmentioning

confidence: 99%

Osteoprotegerin and RANKL-RANK-OPG-TRAIL signalling axis in heart failure and other cardiovascular diseases

et al. 2021

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Osteoprotegerin (OPG) is a glycoprotein involved in the regulation of bone remodelling. OPG regulates osteoclast activity by blocking the interaction between the receptor activator of nuclear factor kappa B (RANK) and its ligand (RANKL). More and more studies confirm the relationship between OPG and cardiovascular diseases. Numerous studies have confirmed that a high plasma concentration of OPG and a low concentration of tumour necrosis factor–related apoptosis inducing ligand (TRAIL) together with a high OPG/TRAIL ratio are predictors of poor prognosis in patients with myocardial infarction. A high plasma OPG concentration and a high ratio of OPG/TRAIL in the acute myocardial infarction are a prognostic indicator of adverse left ventricular remodelling and of the development of heart failure. Ever more data indicates the participation of OPG in the regulation of the function of vascular endothelial cells and the initiation of the atherosclerotic process in the arteries. Additionally, it has been shown that TRAIL has a protective effect on blood vessels and exerts an anti-atherosclerotic effect. The mechanisms of action of both OPG and TRAIL within the cells of the vascular wall are complex and remain largely unclear. However, these mechanisms of action as well as their interaction in the local vascular environment are of great interest to researchers. This article presents the current state of knowledge on the mechanisms of action of OPG and TRAIL in the circulatory system and their role in cardiovascular diseases. Understanding these mechanisms may allow their use as a therapeutic target in cardiovascular diseases in the future.

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Tumor Necrosis Factor Related Apoptosis Inducing Ligand (Trail) in Endothelial Response to Biomechanical and Biochemical Stresses in Arteries

Cited by 14 publications

References 48 publications

The Role of Osteoprotegerin and Its Ligands in Vascular Function

The Role of Osteoprotegerin and Its Ligands in Vascular Function

Recombinant Bcl-xL attenuates vascular hyperpermeability in a rat model of hemorrhagic shock

Osteoprotegerin and RANKL-RANK-OPG-TRAIL signalling axis in heart failure and other cardiovascular diseases

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