Research paperModified low density lipoprotein and cytokines mediate monocyte adhesion to smooth muscle cells
References (47)
- et al.
Protein measurement with the Folin Phenol reagent
J Biol Chem
(1951) Assay for serum lipid peroxide level and its clinical significance
- et al.
Oxidised low density lipoprotein is chemotactic for arterial smooth muscle cells in culture
FEBS
(1990) - et al.
Biologically modified LDL increases the adhesive properties of endothelial cells
Atherosclerosis
(1991) Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity
Cell
(1991)- et al.
Characterisation of the promoter for vascular cell adhesion molecule-1 (VCAM-1)
J Biol Chem
(1992) - et al.
Enhancement of monocyte adhesion to endothelial cells by oxidatively modified LDL is mediated by activation of CD11b
Biochem Biophs Res Commun
(1995) - et al.
Influence of plaque configuration and stress distribution and fissuring on coronary atherosclerotic plaques
Lancet
(1989) The pathogenesis of atherosclerosis: a perspective for the 1990s
Nature
(1993)- et al.
Oxidatively modified low density lipoproteins: a potential role in recruitment and retention of monocyte/macrophages during atherogenesis
Intimal hyperplasia as a cause of restenosis after percutaneous transluminal coronary angioplasty
Arch Pathol Lab Med
Expression of intercellular adhesion molecule-1 in atherosclerotic plaques
Am J Pathol
Vascular cell adhesion molecule 1 is expressed in human coronary atherosclerotic plaques
J Clin Invest
Integrins and other cell adhesion molecules
FASEB J
Adhesion of activated T lymphocytes to vascular smooth muscle cells and dermal fibroblasts is mediated by beta 1- and beta 2-integrins
Scand J Immunol
TGF-β and endothelial cells inhibit VCAM-1 expression on vascular smooth muscle cells
Arterioscler Thromb Vasc Biol
Endothelial and smooth muscle cells alter low density lipoprotein in vitro by free radical oxidation
Arteriosclerosis
Superoxides initiate oxidation of low density lipoprotein by monocytes
Arteriosclerosis
Oxidised low density lipoprotein induces differentiation and adhesion of human monocytes and the monocytic cell line U937
Minimally low density lipoprotein stimulates monocyte endothelial interactions
J Clin Invest
Smooth muscle cells from adult human aorta
The extent of oxidative modification of low density lipoprotein determines the degree of cytotoxicity to human coronary artery cells
Heart
Culture of human endothelial cells derived from umbilical veins
J Clin Invest
Cited by (52)
Andrographis paniculata diterpenoids and ethanolic extract inhibit TNFα-induced ICAM-1 expression in EA.hy926 cells
2019, PhytomedicineCitation Excerpt :TNFα, a pro-inflammatory cytokine that triggers the inflammatory activation of ECs, is highly expressed in inflammatory diseases such as atherosclerosis and cancer (Kempe et al., 2005; Wu and Zhou, 2010). Activation of the transcription factor NFκB by TNFα is intimately associated with inflammation through increases in the expression of pro-inflammatory cytokines including IL-1 and MCP-1 as well as adhesion molecules like ICAM-1 (Collins et al., 1995; Thorne et al., 1996). TNFα has been shown to up-regulate the expression of ICAM-1 through a TNFR1/TRAF2/PKCδ/JNK1/2-dependent c-Jun signaling pathway in retinal pigment epithelial cells (Lee et al., 2015).
Prevalence of Panoramically Imaged Carotid Atheromas in Alcoholic Patients With Chronic Pancreatitis and Comorbid Diabetes
2018, Journal of Oral and Maxillofacial SurgeryCitation Excerpt :These macrovascular lesions likely resulted from both the inflammatory component of the underlying disorder and the associated metabolic disorder. Specifically, cytokines such as tumor necrosis factor α in the pancreatic tissues spill over into the systemic circulation and promote an atherogenic milieu (increased permeability of endothelial cells, monocyte adhesion, macrophage differentiation, vascular smooth muscle cell proliferation, foam cell formation, and calcification of vascular cells).28-35 Further promoting the atherogenic process is the comorbid diabetic environment characterized by hyperglycemia, with a deficiency in vascular protective high-density lipoprotein level and heightened oxidative modification of the admittedly lower low-density lipoprotein level.36,37
Sphingosylphosphorylcholine inhibits macrophage adhesion to vascular smooth muscle cells
2016, Biochemical PharmacologyCitation Excerpt :While research has focussed on the mechanisms of monocyte/macrophage adhesion to endothelial cells, relatively little attention has been paid to interaction of monocyte/macrophage with vascular SMC. Evidence now indicates that monocyte/macrophage adhesion to vascular SMC is likely to be involved in the initiation of vascular disease [7,8]. It is clear that macrophages and vascular SMC are in direct contact in atherosclerotic plaque regions of human blood vessels [9].
Correlation between lipid deposition, immune-inflammatory cell content and MHC class II expression in diffuse intimal thickening of the human aorta
2011, AtherosclerosisCitation Excerpt :On the 5th day of cell cultivation, native LDL and nomLDL (100 μg apoB/ml) were added and the cells were cultivated with the LDL for 24 h. Following this incubation, intracellular cholesterol level, HLA-DR expression and the production of tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) were measured. The induction of HLA-DR, TNF-α and IL-1 by LDL was quantified using a cell-based ELISA technique according to Thorne et al. [48]. The data were analyzed using the SPSS statistical package (SPSS Inc., version 14.0, USA).
Carbamylated LDL
2010, Advances in Clinical ChemistryCitation Excerpt :The cLDL-induced synthesis of the LOX-1 protein significantly contributes to both cytotoxicity and accelerated monocyte adhesion to endothelial cells. Modified LDLs mediate monocyte adhesion to smooth-muscle cells [150]. cLDL significantly induces VSMC proliferation and increases ICAM-1 and VCAM-1 expression [151].
- ∗
Present address: Cardiothoracic Unit, Great Ormond Street Hospital for Sick Children, Great Ormond Street, London WC1N 3JH, UK; Tel.: +44 0171 4059200; fax: +44 0171 8298673.