CX3CR1 receptor is up-regulated in monocytes of coronary artery diseased patients: Impact of pre-inflammatory stimuli and renin–angiotensin system modulators

Apostolakis, Stavros; Krambovitis, Elias; Vlata, Zaharenia; Kochiadakis, Georgios E.; Baritaki, Stavroula; Spandidos, Demetrios Α.

doi:10.1016/j.thromres.2007.04.005

Cited by 34 publications

(30 citation statements)

References 42 publications

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“…The authors further demonstrated that statin therapy for 6 months reduced the expression of CX3CL1 and CX3CR1 [38] . Our group, using flow cytometry, similarly observed a higher rate of CX3CR1-positive peripheral blood mononuclear cells in patients with coronary artery disease as compared to the controls with a difference that was enhanced beyond the limit of statistical significance when CX3CR1 expression was evaluated in the monocyte gate [39] . In a different cardiovascular disease setting, Richter et al assessed CX3CL1 plasma levels in 349 patients with advanced systolic heart failure.…”

Section: Wwwnaturecom/aps Apostolakis S Et Almentioning

confidence: 54%

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

2013

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Atherosclerosis is currently considered an inflammatory disease. Much attention has been focused on the potential role of inflammatory mediators as prognostic/diagnostic markers or therapeutic targets of atherosclerotic cardiovascular disease. CX3CL1 (or fractalkine) is a structurally and functionally unique chemokine with a well documented role in atherosclerosis. In its membrane bound form it promotes the firm adhesion of rolling leucocytes onto the vessel wall, while in its soluble form it serves as a potent chemoattractant for CX3CR1-expressing cells. Additionally, CX3CL1 exerts cytotoxic effects on the endothelium as well as anti-apoptotic and proliferative effects on vascular cells, affecting the context and stability of the atherosclerotic plaque. Studies on animal models have shown that the blockade of the CX3CL1/CX3CR1 pathway ameliorates the severity of atherosclerosis, while genetic epidemiology has confirmed that a genetically-defined less active CX3CL1/CX3CR1 pathway is associated with a reduced risk of atherosclerotic disease in humans. Although several studies support an important pathogenic role of CX3CL1/CX3CR1 in atherogenesis and plaque destabilization, this does not necessarily suggest that this pathway is a suitable therapeutic target or that CX3CL1 can serve as a prognostic/ diagnostic biomarker. Further studies on the CX3CL1/CX3CR1 chemokine pathway are clearly warranted to justify the clinical relevance of its role in atherosclerosis.

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Section: Wwwnaturecom/aps Apostolakis S Et Almentioning

confidence: 54%

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

2013

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“…24,39 The differential effects displayed by Ang-II in each type of endothelia suggest that CX 3 CL1 is crucial for mononuclear cell adhesion to the arterial endothelium, whereas CX 3 CL1 acts in combination with other components Published studies have reported increased CX 3 CR1 expression in circulating monocytes of patients with coronary artery disease. 18 Furthermore, a genetic polymorphism found in the gene encoding the human CX 3 CL1 receptor, CX 3 CR1-M280, was associated with a decreased risk of atherosclerosis in heterozygote individuals. 16,17 Because Ang-II levels are elevated in many cardiovascular diseases 1,2 and human mononuclear cells express the Ang-II AT 1 receptor, the potential upregulation of CX 3 CR1 in human monocytes and lymphocytes by Ang-II was also investigated.…”

Section: Discussionmentioning

confidence: 99%

“…16,17 More recently, CX 3 CR1 upregulation has been detected in circulating monocytes of patients with coronary artery disease. 18 Despite intensive research, the precise molecular mechanisms by which Ang-II exerts differential leukocyte recruitment in arterial and venous endothelia remain largely unknown. Given that CX 3 CL1 is a potent chemoattractant for monocytes and T cells but not for neutrophils 10 and because TNFα is the main inducer of CX 3 CL1 expression in endothelial cells, 19 we have investigated the potential involvement of CX 3 CL1 in the arterial mononuclear cell recruitment induced by Ang-II.…”

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confidence: 99%

Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX ₃ CL1) Expression by Angiotensin-II

Rius

Piqueras²,

González-Navarro³

et al. 2013

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Objective-Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results-Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization of CX 3 CL1 activity only significantly inhibited Ang-II-induced mononuclear cell-human umbilical arterial endothelial cell interactions (73%) but not with human umbilical venous endothelial cells. The use of small interfering RNA revealed the involvement of tumor necrosis factor-α in Ang-II-induced CX 3 CL1 upregulation and mononuclear cell arrest. Nox5 knockdown with small interfering RNA or pharmacological inhibition of extracellular signal-regulated kinases1/2, p38 mitogen-activated protein kinase, and nuclear factor-κB also abolished these responses. Finally, when human umbilical arterial endothelial cells were costimulated with Ang-II, tumor necrosis factor-α, and interferon-γ, CX 3 CL1 expression and mononuclear cell adhesiveness were more pronounced than when each stimulus was provided alone. Conclusion-These

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“…In a recent study of ours, higher rates of CX3CR1-positive monocytes were observed in CAD patients as compared to subjects with normal coronary angiography. Furthermore, we demonstrated in vitro that a pre-inflammatory environment induced by INF-gamma enhances the rate and fluorescence intensity of CX3CR1-positive THP-1 monocytes, indicating that regulation of the chemokine system occurs not only at the level of agonist production, but also at the level of CX3CR1 receptor expression [58] . Studies have also implicated CX3CL1 in platelet stimulation and activation.…”

Section: Cx3cl1 and Cx3c Receptormentioning

confidence: 84%

Therapeutic implications of chemokine-mediated pathways in atherosclerosis: realistic perspectives and utopias

2010

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Current perspectives on the pathogenesis of atherosclerosis strongly support the involvement of inflammatory mediators in the establishment and progression of atherosclerostic lesions. Chemokine-mediated mechanisms are potent regulators of such processes by orchestrating the interactions of inflammatory cellular components of the peripheral blood with cellular components of the arterial wall. The increasing evidence supporting the role of chemokine pathways in atherosclerosis renders chemokine ligands and their receptors potential therapeutic targets. In the following review, we aim to highlight the special structural and functional features of chemokines and their receptors in respect to their roles in atherosclerosis, and examine to what extent available data can be applied in disease management practices.

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CX3CR1 receptor is up-regulated in monocytes of coronary artery diseased patients: Impact of pre-inflammatory stimuli and renin–angiotensin system modulators

Cited by 34 publications

References 42 publications

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX ₃ CL1) Expression by Angiotensin-II

Therapeutic implications of chemokine-mediated pathways in atherosclerosis: realistic perspectives and utopias

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CX3CR1 receptor is up-regulated in monocytes of coronary artery diseased patients: Impact of pre-inflammatory stimuli and renin–angiotensin system modulators

Cited by 34 publications

References 42 publications

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

Therapeutic implications of chemokine-mediated pathways in atherosclerosis: realistic perspectives and utopias

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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX ₃ CL1) Expression by Angiotensin-II