The Relationship of Various Factors in the Pathogenesis of Atherosclerosis

Sönmez, Hüseyin; Süer, Selma; Ulutin, Turgut; Kökoğlu, Emine; Üçişik, Nergiz

doi:10.1177/107602969800400205

Cited by 9 publications

(5 citation statements)

References 54 publications

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“…In addition, lipoprotein (a) and LDL bound to fibronectin is internalized through the fibronectin receptor pathway and thereby causes increased accumulation of lipid, and foam cell formation (18). Stenman and colleagues (19) observed prominent immunofluorescent staining for FN in early cellular atherosclerotic lesions of human muscular arteries, which may suggest that excessive production contributes to the pathogenesis of atherosclerotic cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Fibronectin, Vitronectin, and Leptin Levels in Coronary Artery Disease: Impacts on Thrombosis and Thrombolysis

Ekmekçi

Sönmez

et al. 2005

Clin Appl Thromb Hemost

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In this study, the levels of fibronectin, vitronectin, leptin, tissue plasminogen activator (t-PA), and lipid parameters were investigated in patients with coronary artery disease (CAD) and control group. The average plasma fibronectin levels in CAD patients group were significantly higher compared with the control group (p=0.006). Moreover, in patients with triple-vessel disease, plasma fibronectin levels were found to be significantly higher than those in the control group (p<0.05). Plasma vitronectin levels in patients with CAD were found to be significantly higher than those in the control group (p=0.000). In addition, in patients with double vessel disease plasma vitronectin levels were significantly higher than no vessel disease and control group, triple vessel disease was significantly higher as compared with no vessel disease, single vessel disease, and control group (p<0.05). We could not find any significant differences in t-PA values between CAD patients and control group. On the other hand, the average leptin levels in the group of patients were higher than those in the control group but there were no statistically significant differences found between them (p>0.05) because of high SD values. There was strong (+) correlation between fibronectin, vitronectin, and severity of disease [vitronectin/severity of disease, r = 0.5074 (p = 0.000), fibronectin/severity of disease, r = 0.2971 (p = 0.007)]. In conclusion, we can say that fibronectin and vitronectin have become greatly important in pathogenesis of coronary artery disease. High leptin levels may be contribute to platelet aggregation in patients with coronary artery disease. But, elevated serum levels of leptin cannot be useful diagnostic and monitoring markers in patients with coronary artery disease.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Fibronectin, Vitronectin, and Leptin Levels in Coronary Artery Disease: Impacts on Thrombosis and Thrombolysis

Ekmekçi

Sönmez

et al. 2005

Clin Appl Thromb Hemost

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“…Diabetes-and infection-related inflammations are major predisposing factors for vascular disorders [38,39]. Both these conditions are known to release neuraminidases [40,41] that can cause desialylation of host cells and render them receptors for cell-reactive Lp(a)-IC that are concomitantly produced. In this context, a notable observation was that in animal models lesion-prone areas of arterial wall were relatively more desialylated [42].…”

Section: Discussionmentioning

confidence: 99%

Immunopathology of desialylation: human plasma lipoprotein(a) and circulating anti-carbohydrate antibodies form immune complexes that recognize host cells

Sabarinath

Appukuttan

2015

Mol Cell Biochem

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Human plasma lipoprotein(a) [Lp(a)], the dominant lipoprotein in atherosclerotic plaques, contains an apo(a) subunit of variable size linked to the apoB subunit of a low-density lipoprotein (LDL) molecule. Circulating lipoprotein immune complexes (ICs) assayed by ELISA using microplate-coated anti-apo(a) or anti-apoB antibody for capture and peroxidase-labelled anti-human immunoglobulins as probe consisted mostly of Lp(a) despite several-fold excess of LDL over Lp(a) in plasma. Microplate coating of plasma lipoprotein IC and probing with antibodies to apo(a) and apoB also revealed negligible presence of LDL compared to Lp(a). Peanut agglutinin specific to desialylated O-glycans bound significantly more to Lp(a) recovered after urea dissociation of IC than to free Lp(a). Plasma lipoproteins separated by ultracentrifugation and desialylated by neuraminidase formed IC with naturally occurring antibodies in normal plasma. These de novo ICs agglutinated desialylated but not normal human RBC in proportion to the polyagglutinin antibody titre of plasma used, suggesting availability of multiple unoccupied binding sites on the participating antibodies even after IC formation. Agglutination was inhibitable by galactosides and decreased 4-8 fold if precursor lipoprotein was selectively depleted of Lp(a), showing agglutinating ICs were contributed mainly by desialylated Lp(a) and galactose-specific antibodies. IC was 2 fold more agglutinating if lipoproteins used contained smaller rather than larger Lp(a) molecules of the same number. Small size/high plasma concentration Lp(a) phenotype and neuraminidase-releasing diseases including diabetes are risk factors for vascular disorders. Results suggest a possible route of Lp(a) attachment to vascular cells that offer terminal galactose on surface glycans following desialylation.

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“…While serum contains several fold higher concentration of LDL than Lp(a), atherosclerotic plaques have been reported to contain more apo(a) than apoB with increase in levels of apo(a) during plaque progression . While serum neuraminidase levels are elevated in patients with coronary heart diseases , studies also reveal that Lp(a) from such patients are 2.5‐fold more desialylated than from normal subjects and that desialylated Lp(a) forms aggregates in human aortic intimal cells . However, response of circulating immunoglobulins to desialylated Lp(a) and mechanism of tissue deposition of the lipoprotein remain unexplored.…”

Section: Discussionmentioning

confidence: 99%

Dual Specificity of Human Plasma Lactose‐Binding Immunoglobulin to Anomers of Terminal Galactose Enables Recognition of Desialylated Lipoprotein(a) and Xenoantigens

2014

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Human plasma lactose-binding immunoglobulin (LIg) isolated by affinity chromatography on lactose-Sepharose was largely IgG with significant IgA and IgM contents. LIg-mediated agglutination of desialylated human RBC was inhibited equally by the a-and b-anomers of methyl galactoside. Recognition of either the terminal a-galactose (TAG)-containing glycans of bovine thyroglobulin or the N-acetyl lactosamine (LacNAc)-terminating glycans of asialofetuin by LIg was inhibitable nearly as much by the a-galactoside melibiose as by the b-galactoside lactose. Melibiose covalently conjugated to protein and coated on polystyrene wells captured several times more LIg molecules than its lactose analogue. LIg binding to bovine thyroglobulin or rabbit RBC membrane proteins, both bearing TAG was substantially reduced by prior treatment of the proteins with a-galactosidase to remove TAG though enzyme-treated glycans contained newly exposed LacNAc moieties. Desialylated O-linked oligosaccharides, however, were no ligand for LIg. Unlike LDL, plasma lipoprotein(a) [Lp(a)] coated on polystyrene well and desialylated by neuraminidase was recognized by LIg through terminal LacNAc moieties exposed by the enzyme on its apo(a) subunit. Further, same amount of added fluorescence-labelled LIg formed significantly more immune complex with Lp(a) in high Lp(a) plasma than in low Lp(a) plasma. Results suggest (1) possibility of a role for LIg in combating nonprimate molecules and cells bearing TAG moiety and (2) a mechanism for Lp(a)-mediated vascular injury as diabetes, infections and inflammations induce greater release of neuraminidase into circulation.

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The Relationship of Various Factors in the Pathogenesis of Atherosclerosis

Cited by 9 publications

References 54 publications

Evaluation of Fibronectin, Vitronectin, and Leptin Levels in Coronary Artery Disease: Impacts on Thrombosis and Thrombolysis

Evaluation of Fibronectin, Vitronectin, and Leptin Levels in Coronary Artery Disease: Impacts on Thrombosis and Thrombolysis

Immunopathology of desialylation: human plasma lipoprotein(a) and circulating anti-carbohydrate antibodies form immune complexes that recognize host cells

Dual Specificity of Human Plasma Lactose‐Binding Immunoglobulin to Anomers of Terminal Galactose Enables Recognition of Desialylated Lipoprotein(a) and Xenoantigens

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