Insulin-like growth factor 1 opposes the effects of C-reactive protein on endothelial cell activation

2013 ◽  
Vol 385 (1-2) ◽  
pp. 199-205 ◽  
Author(s):  
Shao-Jun Liu ◽  
Yun Zhong ◽  
Xiang-Yu You ◽  
Wei-Hua Liu ◽  
Ai-Qun Li ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Activation ◽  
Insulin Like Growth Factor ◽  
C Reactive Protein ◽  
Endothelial Cell Activation ◽  
Reactive Protein

Circulating Levels of High-Sensitivity C-Reactive Protein and Soluble Markers of Vascular Endothelial Cell Activation in Growth Hormone-Deficient Adolescents

2008 ◽  
Vol 70 (4) ◽  
pp. 230-235 ◽  
Author(s):  
Roberto Lanes ◽  
Henry Marcano ◽  
Omar Villaroel ◽  
Peter Gunczler ◽  
Edgar Morillo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Vascular Endothelial Cell ◽  
High Sensitivity ◽  
Vascular Endothelial ◽  
C Reactive Protein ◽  
Endothelial Cell Activation ◽  
Reactive Protein ◽  
Circulating Levels

Endothelial dysfunction as a possible link between C-reactive protein levels and cardiovascular disease

2000 ◽  
Vol 98 (5) ◽  
pp. 531-535 ◽  
Author(s):  
Stephen J. CLELAND ◽  
Naveed SATTAR ◽  
John R. PETRIE ◽  
Nita G. FOROUHI ◽  
Henry L. ELLIOTT ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Cell Activation ◽  
Density Lipoprotein ◽  
Low Grade ◽  
C Reactive Protein ◽  
Endothelial Cell Activation ◽  
Reactive Protein ◽  
The Relationship

Low-grade chronic inflammation, characterized by elevated plasma concentrations of C-reactive protein (CRP), is associated with an increased risk of atherosclerotic cardiovascular disease. Endothelial cell activation is an early event in atherogenesis, and previous studies have reported correlations between indirect markers of endothelial cell activation and CRP concentration. Therefore, in the present study, we measured CRP concentration (and leptin concentration as an index of fat mass) in nine healthy subjects (mean age 53±8.1 years; body mass index 27±3.2 kg/m2; mean arterial blood pressure 101±9.0 mmHg) undergoing measurement of basal endothelial nitric oxide (NO) synthesis using intra-brachial infusions of NG-monomethyl-l-arginine (l-NMMA; a substrate inhibitor of endothelial NO synthase) and noradrenaline (a non-specific control vasoconstrictor). In univariate analysis, CRP concentration was correlated with (i) the percentage decrease in forearm blood flow (FBF) during l-NMMA infusion (r = 0.85, P = 0.004); and (ii) the serum leptin concentration (r = 0.65, P = 0.05). In multivariate analysis, the relationship between CRP concentration and the FBF response to l-NMMA remained significant when age and leptin (t = 2.65, P = 0.045), age and BMI (t = 3.69, P = 0.014), or age and low-density-lipoprotein-cholesterol plus high-density-lipoprotein-cholesterol (t = 3.37, P = 0.044), were included in regression models. In contrast, the response of FBF to noradrenaline was not significantly related to CRP concentration. These data demonstrate for the first time a relationship between low-grade chronic inflammation and basal endothelial NO synthesis (measured using an invasive method), and support the notion that endothelial dysfunction is a critical intermediate phenotype in the relationship between inflammation and cardiovascular disease.

Glycogen synthase kinase-3β is involved in C-reactive protein-induced endothelial cell activation

2013 ◽  
Vol 78 (8) ◽  
pp. 915-919
Author(s):  
Shao-Jun Liu ◽  
Wei-Hua Liu ◽  
Yun Zhong ◽  
Shi-Ming Liu
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase ◽  
Glycogen Synthase Kinase 3Β ◽  
C Reactive Protein ◽  
Endothelial Cell Activation ◽  
Reactive Protein

scholarly journals C-Reactive Protein–Induced In Vitro Endothelial Cell Activation Is an Artefact Caused by Azide and Lipopolysaccharide

2005 ◽  
Vol 25 (6) ◽  
pp. 1225-1230 ◽  
Author(s):  
Karolina E. Taylor ◽  
John C. Giddings ◽  
Carmen W. van den Berg
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
C Reactive Protein ◽  
Endothelial Cell Activation ◽  
Reactive Protein

scholarly journals Endothelial cell-activating antibodies in COVID-19

2021 ◽  
Author(s):  
Hui Shi ◽  
Yu Zuo ◽  
Alex A. Gandhi ◽  
Gautam Sule ◽  
Srilakshmi Yalavarthi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Activation ◽  
Neutrophil Extracellular Trap ◽  
C Reactive Protein ◽  
Serum Samples ◽  
Endothelial Cell Activation ◽  
Reactive Protein ◽  
Control Serum ◽  
Vascular Beds

ABSTRACTPatients with coronavirus disease 19 (COVID-19) are at high risk for fibrin-based occlusion of vascular beds of all sizes. Although endothelial cell activation has regularly been described as part of the COVID-19 thrombo-inflammatory storm, the upstream mediators of this activation have yet to be fully elucidated. Here, we began by pursuing the hypothesis that circulating factors such as neutrophil extracellular trap (NET) remnants, D-dimer, or C-reactive protein might predict the COVID-19 serum samples (n=118) that most robustly activated cultured endothelial cells. Indeed, we found modest correlations between serum NET remnants (cell-free DNA, myeloperoxidase-DNA complexes, citrullinated histone H3) and upregulation of surface E-selectin, VCAM-1, and ICAM-1 on endothelial cells. However, a more robust predictor of the ability of COVID-19 serum to activate endothelial cells was the presence of circulating antiphospholipid antibodies, specifically anticardiolipin IgG and IgM and anti-phosphatidlyserine/prothrombin (anti-PS/PT) IgG and IgM. Depletion of total IgG from anticardiolipin-high and anti-PS/PT-high samples markedly restrained upregulation of E-selectin, VCAM-1, and ICAM-1. At the same time, supplementation of control serum with patient IgG was sufficient to trigger endothelial cell activation. These data are the first to reveal that patient antibodies are a driver of endothelial cell activation and add important context regarding thrombo-inflammatory effects of COVID-19 autoantibodies in severe COVID-19.

scholarly journals A substitution model of dietary manipulation is an effective means of optimising lipid profile, reducing C-reactive protein and increasing insulin-like growth factor-1

2004 ◽  
Vol 92 (5) ◽  
pp. 809-818 ◽  
Author(s):  
Adrian H. Heald ◽  
Cheryl Golding ◽  
Reena Sharma ◽  
Kirk Siddals ◽  
Sara Kirk ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dietary Intervention ◽  
Short Interval ◽  
The Other ◽  
Fat Intake ◽  
Insulin Like Growth Factor ◽  
C Reactive Protein ◽  
High Fat ◽  
Substitution Model ◽  
Reactive Protein

There are two key methods in which fat intake may be manipulated; the ‘substitution model’ and the ‘reduction model’. However insufficient information is known about the mechanisms of dietary fat reduction in individuals who have successfully reduced their fat intake, to be clear as to which strategy offers the greatest chance of success. Our objective was to ascertain the most effective dietary intervention for improving cardiovascular risk profile. Eighty female volunteers (high fat consumers) were recruited. Each subject was randomly allocated into one of the following groups. Substitution of high-fat foods was made with reduced-fat products, by the reduction of high-fat foods, by a combination of substitution and reduction strategies, or no advice was given. Each intervention lasted 3 months. Anthropometric measures and fasting blood samples were taken at baseline and follow-up. The substitution intervention resulted in weight loss (mean −1.4 (95% CI −2.4, −0.2) kg) and reduced percentage body fat (mean −1.3 (95% CI −2.0, −0.5)%). There was no significant weight change with the other interventions. Fasting triacylglycerols (−0.2 (SEM 0.07) mM; P=0.04), cholesterol and C-reactive protein (CRP) levels (0.8 (SEM 0.2) mg/l; P=0.04) fell with the substitution intervention, but not with the other interventions. Insulin-like growth factor-1 increased with both substitution and reduction (P=0.02). There was no significant change in fasting insulin or glucose with any intervention. The substitution model of dietary intervention is effective even over a relatively short interval of time in reducing fasting total cholesterol, triacylglycerols and CRP. Although the group size for the present study was small and involved females only, it has significant implications for population intervention strategies.

Total Serum Insulin-like Growth Factor-1 and C-Reactive Protein in Metabolic Syndrome With or Without Diabetes

Angiology ◽  
2006 ◽  
Vol 57 (3) ◽  
pp. 303-311 ◽  
Author(s):  
Georgios Efstratiadis ◽  
Georgios Tsiaousis ◽  
Vasilios G. Athyros ◽  
Despina Karagianni ◽  
Aikaterini Pavlitou-Tsiontsi ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Growth Factor ◽  
Serum Insulin ◽  
Total Serum ◽  
Insulin Like Growth Factor ◽  
C Reactive Protein ◽  
Reactive Protein

Role of Connective Tissue Growth Factor In Endothelin-Mediated Endothelial Cell Activation

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2107-2107
Author(s):  
Anna J Hernandez ◽  
Sonia Henriquez ◽  
Enrique R Maldonado ◽  
Rodeler Youte ◽  
Gregory N Prado ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factors ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Connective Tissue ◽  
Cell Activation ◽  
Fold Increase ◽  
Tissue Growth ◽  
Vegf Expression ◽  
Endothelial Cell Activation

Abstract Abstract 2107 Endothelial cell activation and elevated levels of circulating Endothelin-1 (ET-1) have been reported in patients with atherosclerosis and sickle cell disease (SCD). ET-1 is a well-described vasoconstrictor, mitogen and regulator of endothelial cells migration that has been shown to promote structural changes in blood vessels. ET-1 is produced in response to increases in vasoactive hormones, growth factors, hypoxia, shear stress and free radicals, events that are commonly observed in patients with SCD. Endothelial cell activation is in part characterized by increases of cytokines such as monocyte chemotactic protein-1 (MCP-1) and growth factors that are important in vascular maintenance and fibrogenesis such as connective tissue growth factor (CTGF) and vascular endothelial growth factor (VEGF). CTGF and VEGF are important for blood vessel remodeling, fibrogenesis and angiogenesis. Indeed there is evidence that incubation of smooth muscle cells with ET-1 leads to increases in CTGF and VEGF levels. However, the relationship between ET-1 and CTGF in endothelial cell activation is unclear. We hypothesize that increasing ET-1 would stimulate CTGF production and endothelial cell activation. We studied the effects of ET-1 on the human endothelial cell line, EA.hy926 (EA), as well as in primary cultures of mouse aortic endothelial cells (MAEC). We performed gene expression time course experiments (0, 2, 4, 8, 16, 24 Hr) on EA cells following incubation with 100nM ET-1 using quantitative RT-PCR with Taqman chemistries and GAPDH and beta-actin as endogenous controls. We observed increases of CTGF and VEGF expression between 4 and 8 hr for CTGF (1.74 fold increase vs time 0, n=6, P<0.03) and 4 hr for VEGF (2.14 fold increase vs time 0, n=3, P<0.04). Additional experiments on EA cells showed that incubation with 100nM ET-1 for 4 hr in the presence of BQ123 and BQ788, two inhibitors of ET-1 type A and B receptors, respectively, blocked the ET-1 stimulated rises in CTGF and VEGF as well as MCP-1 expression. We then performed western blot analyses (Abcam-CTGF antibody ab6992; Abcam VEGF antibody ab1316) and showed increases in cell associated CTGF protein levels following incubation of EA cells with 100nM ET-1 for 24 hr. The ET-1 stimulated rise in CTGF levels were significantly blunted by pre-incubation of EA cells with both BQ788 and BQ123. To study whether the effects of ET-1 were unique to EA cells, we also analyzed the effects of ET-1 on early cultures of MAEC isolated from C57BLJ mice. Consistent with our observations in human endothelial cells, incubation of MAEC with 100nM ET-1 for 4 hr were associated with increases of CTGF and VEGF expression (1.86 fold vs vehicle, n=3, P<0.03; 1.73 fold vs vehicle, n=3 P<0.04 respectively). Furthermore, ET-1 stimulated rises in CTGF and VEGF expressions were likewise blocked by pre-incubation with BQ123 andBQ788. We conclude that addition of ET-1 leads to activation of endothelial cells and increases in CTGF and VEGF from human and mouse endothelial cells. Thus we suggest that therapies designed to block ET-1 receptors will reduce endothelial cell activation in part by reducing CTGF production leading to alterations in cellular and tissue architecture. This work was supported by NIH R01HL090632 to AR and R01HL096518 to JRR. Disclosures: No relevant conflicts of interest to declare.

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