scholarly journals Dietary Antioxidants Decrease Serum Soluble Adhesion Molecule (sVCAM-1, sICAM-1) but not Chemokine (JE/MCP-1, KC) Concentrations, and Reduce Atherosclerosis in C57BL but Not ApoE*3 Leiden Mice Fed an Atherogenic Diet

2005 ◽  
Vol 21 (4) ◽  
pp. 181-190 ◽  
Author(s):  
Nuala Murphy ◽  
David C Grimsditch ◽  
Martin Vidgeon-Hart ◽  
Pieter H.E. Groot ◽  
Philip Overend ◽  
...  
Keyword(s):  
Adhesion Molecules ◽  
Atherosclerotic Lesion ◽  
Transgenic Animals ◽  
Serum Levels ◽  
Lesion Size ◽  
Atherogenic Diet ◽  
Initial Increase ◽  
Dietary Antioxidants ◽  
Soluble Adhesion Molecules ◽  
Cellular Expression

Dietary antioxidants are reported to suppress cellular expression of chemokines and adhesion molecules that recruit monocytes to the artery wall during atherosclerosis. In the present study we measured the effect of feeding apoE*3 Leiden mice or their non-transgenic (C57BL) littermates with atherogenic diets either deficient in, or supplemented with, dietary antioxidants (vitamin E, vitamin C and β-carotene) for 12 weeks, on serum levels of CC (JE/MCP-1) and CXC (KC) chemokines and soluble adhesion molecules (sVCAM-1, sICAM-1) and atherosclerotic lesion size. ApoE*3 Leiden mice developed gross hypercholesterolaemia, and markedly accelerated (10–20 fold;P< 0.0001) atherogenesis, compared with non-transgenic animals. Antioxidant consumption reduced lesion area in non-transgenic, but not apoE*3 Leiden, mice. Serum sVCAM-1 and sICAM-1 levels were significantly (P< 0.0001) increased (sVCAM-1 up to 3.9 fold; sICAM-1 up to 2.4 fold) by 4—8 weeks in all groups, and then declined. The initial increase in the concentration of adhesion molecules was reduced by 38%— 61% (P< 0.05) by antioxidant consumption, particularly in non-transgenic mice. By contrast, serum chemokine levels tended to increase more rapidly from baseline in apoE*3 Leiden mice, compared with non-transgenic animals, but were unaffected by dietary antioxidants. We conclude that dietary antioxidants reduce circulating soluble adhesion molecules and atherosclerosis in C57BL mice.

scholarly journals Levels of soluble cell adhesion molecules in type 2 diabetes mellitus patients with macrovascular complications

2019 ◽  
Vol 48 (4) ◽  
pp. 030006051989385
Author(s):  
Gehan A Hegazy ◽  
Zuhier Awan ◽  
Enayat Hashem ◽  
Nabil Al-Ama ◽  
Asmaa Basha Abunaji
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Serum Levels ◽  
Macrovascular Complications ◽  
Soluble Adhesion Molecules

Objective Type 2 diabetes mellitus (T2DM) is a main risk factor for development of cardiovascular diseases (CVDs) and endothelial dysfunction. This study aimed to investigate serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), intercellular adhesion molecule 1 (sICAM-1), and endothelium selectin (sE-selectin) in T2DM patients with macrovascular complications. Methods A cross-sectional study of 21 controls, 30 T2DM patients without CVDs, and 30 T2DM patients with CVDs was conducted. Serum levels of soluble adhesion molecules including sVCAM-1, sICAM-1, and sE-selectin were determined using ELISA. Results Serum levels of sVCAM-1, sICAM-1, and sE-selectin were higher in T2DM patients than in controls. Levels of serum sVCAM-1 were higher in T2DM patients with CVDs compared with T2DM patients without CVDs. In T2DM patients with CVDs, significant positive associations were observed between sVCAM-1, sICAM-1, and sE-selectin levels (r = 0.575, p = 0.001 and r = 0.378, p = 0.040). Conclusions Circulating levels of soluble adhesion molecules were elevated in T2DM patients, regardless of whether the patients had cardiovascular complications. Only sVCAM-1 was considered a useful marker for the prediction of CVDs in T2DM patients.

Serum Levels of Soluble Adhesion Molecules in Chronic Renal Failure and Dialysis Patients

Nephron ◽  
1998 ◽  
Vol 79 (4) ◽  
pp. 399-407 ◽  
Author(s):  
Mario Bonomini ◽  
Marcella Reale ◽  
Patrizia Santarelli ◽  
Stefano Stuard ◽  
Nicola Settefrati ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Adhesion Molecules ◽  
Serum Levels ◽  
Dialysis Patients ◽  
Soluble Adhesion Molecules

Serum levels of the soluble adhesion molecules in patients with malignant melanoma

2000 ◽  
Vol 6 (1) ◽  
pp. 42-45 ◽  
Author(s):  
Vildan Yasasever ◽  
Faruk Tas ◽  
Derya Duranyildiz ◽  
Hakan Camlica ◽  
Sidika Kurul ◽  
...  
Keyword(s):  
Malignant Melanoma ◽  
Adhesion Molecules ◽  
Serum Levels ◽  
Soluble Adhesion Molecules

scholarly journals Serum Levels of Soluble Adhesion Molecules as Prognostic Factors for Acute Liver Failure

Digestion ◽  
2012 ◽  
Vol 86 (2) ◽  
pp. 122-128 ◽  
Author(s):  
Atsuyuki Ohnishi ◽  
Yasuhiro Miyake ◽  
Hiroshi Matsushita ◽  
Kazuyuki Matsumoto ◽  
Akinobu Takaki ◽  
...  
Keyword(s):  
Prognostic Factors ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Adhesion Molecules ◽  
Serum Levels ◽  
Soluble Adhesion Molecules

scholarly journals Serum levels of soluble adhesion molecules in stem cell transplantation-related complications

2001 ◽  
Vol 27 (9) ◽  
pp. 977-982 ◽  
Author(s):  
Y Matsuda ◽  
J Hara ◽  
Y Osugi ◽  
S Tokimasa ◽  
H Fujisaki ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Adhesion Molecules ◽  
Cell Transplantation ◽  
Serum Levels ◽  
Soluble Adhesion Molecules

Maternal high-fat feeding in pregnancy programs atherosclerotic lesion size in the ApoE*3 Leiden mouse

2016 ◽  
Vol 7 (3) ◽  
pp. 290-297 ◽  
Author(s):  
E. J. Tarling ◽  
K. J. P. Ryan ◽  
R. Austin ◽  
S. J. Kugler ◽  
A. M. Salter ◽  
...  
Keyword(s):  
Plasma Cholesterol ◽  
Maternal Diet ◽  
Atherosclerotic Lesion ◽  
Plasma Lipid ◽  
Lesion Size ◽  
Atherogenic Diet ◽  
Chow Diet ◽  
Wild Type ◽  
High Fat ◽  
Cell Proliferation And Differentiation

Periods of rapid growth seen during the early stages of fetal development, including cell proliferation and differentiation, are greatly influenced by the maternal environment. We demonstrate here that over-nutrition, specifically exposure to a high-fat dietin utero, programed the extent of atherosclerosis in the offspring of ApoE*3 Leiden transgenic mice. Pregnant ApoE*3 Leiden mice were fed either a control chow diet (2.8% fat,n=12) or a high-fat, moderate-cholesterol diet (MHF, 19.4% fat,n=12). Dams were fed the chow diet during the suckling period. At 28 days postnatal age wild type and ApoE*3 Leiden offspring from chow or MHF-fed mothers were fed either a control chow diet (n=37) or a diet rich in cocoa butter (15%) and cholesterol (0.25%), for 14 weeks to induce atherosclerosis (n=36). Offspring from MHF-fed mothers had 1.9-fold larger atherosclerotic lesions (P<0.001). There was no direct effect of prenatal diet on plasma triglycerides or cholesterol; however, transgenic ApoE*3 Leiden offspring displayed raised cholesterol when on an atherogenic diet compared with wild-type controls (P=0.031). Lesion size was correlated with plasma lipid parameters after adjustment for genotype, maternal diet and postnatal diet (R2=0.563,P<0.001). ApoE*3 Leiden mothers fed a MHF diet developed hypercholesterolemia (plasma cholesterol two-fold higher than in chow-fed mothers,P=0.011). The data strongly suggest that maternal hypercholesterolemia programs later susceptibility to atherosclerosis. This is consistent with previous observations in humans and animal models.

scholarly journals Infection with Toxoplasma gondii Increases Atherosclerotic Lesion in ApoE-Deficient Mice

2004 ◽  
Vol 72 (6) ◽  
pp. 3571-3576 ◽  
Author(s):  
Luciane R. Portugal ◽  
Luciana R. Fernandes ◽  
Giovana C. Cesar ◽  
Helton C. Santiago ◽  
Dirce R. Oliveira ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Atherosclerotic Lesion ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Lesion Size ◽  
Liver Cholesterol ◽  
Proinflammatory Response ◽  
Aortic Lesion ◽  
Monocyte Chemoattractant Protein 1 ◽  
Ifn Γ

ABSTRACT Toxoplasma gondii is an intracellular protozoan that elicits a potent inflammatory response during the acute phase of infection. Herein, we evaluate whether T. gondii infection alters the natural course of aortic lesions. ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-γ) were analyzed. Our results showed that serum cholesterol and atherogenic lipoproteins were reduced after T. gondii infection. The reduction of serum levels of total cholesterol and atherogenic lipoproteins was associated with increases in the aortic lesion area, numbers of inflammatory cells, and expression of monocyte chemoattractant protein 1 and inducible nitric oxide synthase mRNA in the site of lesions as well as elevated concentrations of IFN-γ and nitrite in sera of T. gondii-infected animals. These results suggest that infection with T. gondii accelerates atherosclerotic development by stimulating the proinflammatory response and oxidative stress, thereby increasing the area of aortic lesion.

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