Toll-Like Receptor 4 Is Involved in Outward Arterial Remodeling

Hollestelle, Saskia C.G.; Vries, Margreet R. de; Keulen, J. Karlijn van; Schoneveld, Arjan H.; Vink, Aryan; Strijder, Chaylendra; Middelaar, Ben J. van; Pasterkamp, Gérard; Quax, Paul H.A.; Kleijn, Dominique P.V. de

doi:10.1161/01.cir.0000109140.51366.72

Cited by 189 publications

(133 citation statements)

References 38 publications

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“…The first evidence derives from data on the cellular expression and involvement of the TLR-4 signaling pathway in atherosclerotic arteries, and precisely on ECs, macrophages [108,109] and adventitial fibroblasts of these arteries [110]. In 2004, the group of De Kleijn [111], using a femoral artery cuff model in the atherosclerotic ApoE3 (Leiden) transgenic mouse and inducing plaque formation through LPS-mediated TLR-4 activation, demonstrated that the TLR-4 signaling pathway is involved in outward arterial remodeling, probably through up-regulation of TLR-4 itself and its ligands. In 2006, Lin and colleagues [112], by using cell cultures of human aortic smooth muscle cells (HASMCs) from vessels obtained from Zeal and white rabbits treated or without intravenous injections of LPS (110 ng/kg), evidenced that the stimulation of HASMCs with LPS significantly increased the TLR-4 expression.…”

Section: Role Of Tlr-4 Pathway In Aneurysms (Sporadic Taa)?mentioning

confidence: 99%

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Balistreri

Ruvolo

Lio

et al. 2017

Journal of Molecular and Cellular Cardiology

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Section: Role Of Tlr-4 Pathway In Aneurysms (Sporadic Taa)?mentioning

confidence: 99%

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Balistreri

Ruvolo

Lio

et al. 2017

Journal of Molecular and Cellular Cardiology

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“…Evidence that EDA may act as a trigger for atherogenesis is accumulating. EDA levels are elevated in plasma of ApoE knockout mice [23] and EDA mRNA levels are increased during Tlr4-dependent outward remodeling [18]. Furthermore, in atherosclerotic mice lacking EDA, atherosclerotic lesion areas were found to be reduced in number and size [23].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, we and others showed that Tlr4 activation accelerates arterial occlusion by neointima formation, plaque formation, geometrical remodeling and plaque destabilization [18][19][20][21]. It remains unclear which ligands activate Tlr4 and thereby promote atherosclerotic luminal narrowing.…”

Section: Introductionmentioning

confidence: 99%

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Levels of extra domain A containing fibronectin in human atherosclerotic plaques are associated with a stable plaque phenotype

et al. 2007

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Background: Extra domain A (EDA), splice-variant of fibronectin, is a Toll-like receptor 4 (Tlr4) ligand. Recently, EDA has been demonstrated to enhance atherogenesis in mice but human data on the role of EDA in atherosclerotic disease are lacking. We hypothesized that EDA is associated with unstable plaque phenotypes and that plasma EDA could serve as biomarker for atherosclerosis. Methods: EDA levels were assessed in carotid endarterectomy specimen (206 patients) and related with plaque phenotype. In a second patient cohort, systemic EDA levels in atherosclerotic patients (73 patients) were compared to risk-factor matched controls (68 patients).Results: EDA plaque levels were associated with characteristics of stable plaques; more smooth muscle cells (P = 0.003), more collagen (P = 0.071) and less fat (P = 0.023). Concomitantly, asymptomatic patients showed higher EDA values in the plaque compared to symptomatic patients (P = 0.004). EDA plasma levels did not differ between atherosclerotic patients versus controls (P = 0.134). Conclusion: EDA plaque levels are higher in asymptomatic patients and are associated with a stable plaque phenotype. EDA is not a plasma marker for atherosclerotic disease. These results suggest that local presence of endogenous Tlr4 ligand EDA is not associated with in an unstable plaque phenotype in humans.

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“…Notably, enhanced expression of hTLR4 was associated with elevations of IL-1β and TNF-α. Evidence is accumulating that outward arterial remodeling is associated with vulnerable plaque phenotype [19] and increase in hTLR4 expression [20]. Ameziane et al [21] showed that polymorphism of Gly299 allele of the hTLR4 gene is associated with reduction in acute coronary events.…”

Section: Discussionmentioning

confidence: 99%

Association of monoctye expression of Toll-like receptor 4 and its related cytokines with coronary luminal stenosis

Bagheri¹,

Sohrabi²,

Movassaghpur³

et al. 2013

ABB

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Toll-like receptors are well-defined barriers in innate immunity. Among them hTLR4 on the surface of monocytes, plays a critical role in the formation of atherosclerotic plaques, plaque instability and arterial remodeling through production of inflammatory cytokines. This study was designed to examine the association of hTLR4 monocyte expression and response with the severity of coronary stenosis in patients with stable angina (SA). Blood samples were obtained from 39 patients with SA who were scheduled for a coronary angiography and from 28 healthy volunteers. The samples were collected before the procedure. Expression of hTLR4 on CD14 + monocytes and serum levels of TNF-α and IL-1β were measured using flowcytometry and ELISA techniques respectively. Percentage stenosis diameter was measured by comparing the area of coronary stenosis to an adjacent normal segment of the vessel. Compared with control group, patients showed upregulation of hTLR4 + /CD14 + monocytes. Furthermore, patients with more severe coronary stenosis exhibited enhanced expression of hTLR4 + /CD14 + monocytes (p < 0.01). This was paralleled by elevation in the serum levels of TNF-α (p < 0.05) and IL-1β. In addition, significant correlations were seen between percentage stenosis diameter and monocyte expression of hTLR4 as well as TNF-α. hTLR4 monocytic expression and related cytokines are positively associated percentage stenosis diameter. These results suggest that hTLR4 activity may be involved in progression of atherosclerosis.

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Toll-Like Receptor 4 Is Involved in Outward Arterial Remodeling

Cited by 189 publications

References 38 publications

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Levels of extra domain A containing fibronectin in human atherosclerotic plaques are associated with a stable plaque phenotype

Association of monoctye expression of Toll-like receptor 4 and its related cytokines with coronary luminal stenosis

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