Endothelial and leukocyte adhesion molecules in primary hypertriglyceridemia

Benitez, María Belén; Cuniberti, Luis; Fornari, María Cecilia; Rosso, Leonardo Gómez; Berardi, Vanina E.; Elikir, Gerardo; Stutzbach, Pablo; Schreier, Laura; Wikinski, Regina; Brites, Fernando

doi:10.1016/j.atherosclerosis.2007.04.005

Cited by 20 publications

(15 citation statements)

References 43 publications

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“…A crucial factor in monocyte recruitment to atherosclerotic lesions is the level of adhesion molecules expressed on endothelial cells as well as on leucocytes. In a recent study hyperlipidaemia has been directly correlated to a significant increase not only in CAM levels released from endothelial cells but also in some CAMs located at the monocyte surface in human beings [41]. Monocyte CD18 and CD54 showed significantly higher expression in hypertriglyceridemic patients than in controls.…”

Section: Myeloid Cells In Atherosclerosis and Effects Of Hyperlipidaemiamentioning

confidence: 99%

Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Soehnlein

Drechsler

Hristov

et al. 2009

J Cellular Molecular Medi

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Atherosclerosis is a chronic inflammatory disease wherein the infiltration of myeloid cells of the vessel wall is a hallmark event. Lymphocytes, platelets and endothelial cells stand out as prominent suspects being involved in atherosclerosis. However, recent advances suggest a crucial role for myeloid leucocytes, specifically monocyte subsets, neutrophils, dendritic cells and endothelial progenitor cells. These cell types are not just rapidly recruited or already reside in the vascular wall, but also initiate and perpetuate core mechanisms in plaque formation and destabilization. Hyperlipidaemia is an independent risk factor for atherosclerosis. Herein, hyperlipidaemia skews myeloid cell haemostasis, phenotype and transcriptional regulation of pro-inflammatory factors ultimately promoting myeloid cell extravasation and atherosclerosis. We here review the role of myeloid cells in atherosclerosis as well as the effects of hyperlipidaemia on these cells.

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Section: Myeloid Cells In Atherosclerosis and Effects Of Hyperlipidaemiamentioning

confidence: 99%

Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Soehnlein

Drechsler

Hristov

et al. 2009

J Cellular Molecular Medi

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“…It is well established that inflammation plays a pivotal role in the development of classical atherosclerosis, and the inhibition of the expression of adhesion molecules reduces the plaque volume in animal models, probably by reducing the recruitment of monocytes from the blood [8,9] . Patients with primary hyperglyceridemia display increased plasma levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) [10] . Moreover, hyperglycemia induces the increased expression of adhesion molecules in cultured endothelial cells [11] .…”

Section: Introductionmentioning

confidence: 99%

“…Patients with primary hyperglyceridemia display increased plasma levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) [10] . Moreover, hyperglycemia induces the increased expression of adhesion molecules in cultured endothelial cells [11] .…”

Section: Introductionmentioning

confidence: 99%

Felodipine attenuates vascular inflammation in a fructose-induced rat model of metabolic syndrome via the inhibition of NF-κB activation¹

Tan

Shen

et al. 2008

Acta Pharmacologica Sinica

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Aim: Metabolic syndrome is associated with an increased incidence of atherosclerosis. Clinical studies have shown that calcium channel blockers (CCB) inhibit the progression of atherosclerosis. However, the underlying mechanism is unclear. We investigated the inhibitory effect of felodipine on adhesion molecular expression and macrophage infiltration in the aorta of high fructose-fed rats (FFR). Methods: Male Wistar rats were given 10% fructose in drinking water. After 32 weeks of high fructose feeding, they were treated with felodipine (5 mg·kg -1 ·d -1 ) for 6 weeks. The control rats were given a normal diet and water.The aortic expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and the infiltration of macrophages were measured by real-time RT-PCR and/or immunohistochemistry. NF-κB activity was measured by electrophoretic mobility shift assay (EMSA). Results: After 32 weeks of high fructose feeding, FFR displayed increased body weight, systolic blood pressure (SBP), serum insulin, and triglycerides when compared with the control rats. The aortic expressions of ICAM-1 and VCAM-1 were significantly increased in FFR than in the control rats and accompanied by the increased activity of NF-κB. FFR also showed significantly increased CD68-positive macrophages in the aortic wall. After treatment with felodipine, SBP, serum insulin, and the homeostasis model assessment decreased significantly. In addition to reducing ICAM-1 and VCAM-1, felodipine decreased macrophages in the aortic wall. EMSA revealed that felodipine inhibited NF-κB activation in FFR. Conclusion: Felodipine inhibited vessel wall inflammation. The inhibition of NF-κB may be involved in the modulation of vascular inflammatory response by CCB in metabolic syndrome.

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“…The authors noted that postprandial-TRGLs upregulated the expression of several pro-inflammatory genes, including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), P-selectin, interleukin-6 (IL-6), and ADAM metallopeptidase with thrombospondin type 1 (ADAMTS1). [24] Moreover, Benitez et al [25] suggested that increase in leukocyte cell adhesion molecules in primary hypertriglyceridemic subjects would highlight the inflammatory process in the pathogenesis of atherogenesis. Taken in-concert, it is suggested that HTG might be an independent risk factor for endothelial dysfunction and atherosclerosis by virtue of its ability to induce oxidative stress, vascular inflammation, and prothrombotic events in the vessels.…”

Section: Hypertriglyceridemia-associated Endothelial Dysfunction and mentioning

confidence: 98%

Is hypertriglyceridemia a key detrimental factor or associative triggering factor for cardiovascular abnormalities?

Balakumar¹,

Babbar²,

Kalra³

et al. 2012

Syst Rev Pharm

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Endothelial and leukocyte adhesion molecules in primary hypertriglyceridemia

Cited by 20 publications

References 43 publications

Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Felodipine attenuates vascular inflammation in a fructose-induced rat model of metabolic syndrome via the inhibition of NF-κB activation¹

Is hypertriglyceridemia a key detrimental factor or associative triggering factor for cardiovascular abnormalities?

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Endothelial and leukocyte adhesion molecules in primary hypertriglyceridemia

Cited by 20 publications

References 43 publications

Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Felodipine attenuates vascular inflammation in a fructose-induced rat model of metabolic syndrome via the inhibition of NF-κB activation1

Is hypertriglyceridemia a key detrimental factor or associative triggering factor for cardiovascular abnormalities?

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Felodipine attenuates vascular inflammation in a fructose-induced rat model of metabolic syndrome via the inhibition of NF-κB activation¹