Increased plasma adhesion molecule levels in patients with heart failure who have ischemic heart disease and dilated cardiomyopathy

Tousoulis, Dimitris; Homaei, Homeyra; Ahmed, Nabeel; Asimakopoulos, George; Zouridakis, Emmanouil; Toutouzas, Pavlos; Davies, Graham

doi:10.1067/mhj.2001.112683

Cited by 38 publications

(35 citation statements)

References 28 publications

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“…VCAM-1 expression is up-regulated in all of these conditions (29)(30)(31), and all of these tissues recruit EPCs (15,(32)(33)(34)(35). The mechanisms by which EPCs home to these tissues, however, remain poorly elucidated.…”

Section: Discussionmentioning

confidence: 99%

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Silverman¹,

Haas²,

Rad³

et al. 2007

Arthritis & Rheumatism

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Objective. Marrow-derived endothelial progenitor cells (EPCs) are important in the neovascularization that occurs in diverse conditions such as cardiovascular disorders, inflammatory diseases, and neoplasms. In rheumatoid arthritis (RA), synovial neovascularization propels disease by nourishing the inflamed and hyperproliferative synovium. This study was undertaken to investigate the hypothesis that EPCs selectively home to inflamed joint tissue and may perpetuate synovial neovascularization.Methods. In a collagen-induced arthritis (CIA) model, neovascularization and EPC accumulation in mouse ankle synovium was measured. In an antibodyinduced arthritis model, EPC recruitment to inflamed synovium was evaluated. In a chimeric SCID mouse/ human synovial tissue (ST) model, mice were engrafted subcutaneously with human ST, and EPC homing to grafts was assessed 2 days later. EPC adhesion to RA fibroblasts and RA ST was evaluated in vitro.Results. In mice with CIA, cells bearing EPC markers were significantly increased in peripheral blood and accumulated in inflamed synovial pannus. EPCs were 4-fold more numerous in inflamed synovium from mice with anti-type II collagen antibody-induced arthritis versus controls. In SCID mice, EPC homing to RA ST was 3-fold greater than to normal synovium. Antibody neutralization of vascular cell adhesion molecule 1 (VCAM-1) and its ligand component ␣4 integrin potently inhibited EPC adhesion to RA fibroblasts and RA ST cryosections.Conclusion. These data demonstrate the selective recruitment of EPCs to inflamed joint tissue. The VCAM-1/very late activation antigen 4 adhesive system critically mediates EPC adhesion to cultured RA fibroblasts and to RA ST cryosections. These findings provide evidence of a possible role of EPCs in the synovial neovascularization that is critical to RA pathogenesis.

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Section: Discussionmentioning

confidence: 99%

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Silverman¹,

Haas²,

Rad³

et al. 2007

Arthritis & Rheumatism

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“…Such disorders result in imbalance between the load applied to the myocardium and the energy demands for its normal function. Additionally, mediators, such as angiotensin II (AngII), endothelin 1 (ET-1), pro-inflammatory molecules along with increased oxidative stress, act directly or indirectly on the myocardium leading to HF [16,[23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Conflicting effects of nitric oxide and oxidative stress in chronic heart failure: potential therapeutic strategies

Tousoulis

Papageorgiou²,

Briasoulis³

et al. 2011

Heart Fail Rev

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Chronic heart failure (CHF) is characterized by decreased nitric oxide (NO) bioavailability. In addition, the beneficial NO turns to be deleterious when it reacts with superoxide anion, leading to peroxynitrite formation. Numerous experimental and clinical studies have reported increased production of reactive oxygen species (superoxide, hydrogen peroxide, hydroxyl radical) both in animals and patients with CHF. Moreover, there are indicative data suggesting mechanisms associated with endothelial dysfunction in states of CHF, mainly attributed to decreased NO bioavailability and enhanced inactivation of the latter. Thus, such molecules appear to be potential targets in patients with CHF. These patients are strong candidates to receive a variety of therapeutic agents, some of which have known antioxidant effects. Classic treatment with statins or angiotensin converting enzyme inhibitors has been found to be beneficial in restoring NO and improving myocardial function and structure. Other agents such as sildenafil and b-blockers along with novel agents such as NO synthase transcription enhancers have been proved to be also beneficial, but their use for such a purpose is still controversial. Approaches using more-effective antioxidants or targeting myocardial oxidant-producing enzymes and oxidative or nitrosative stress might be promising strategies in the future.

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“…It is known that IL-13 has the ability to selectively induce vascular cell adhesion molecule (VCAM)-1 expression in human endothelial cells [22]. Previous studies have demonstrated that VCAM-1 is closely associated with angiogenesis and have indicated increases in the activities of both myocardial and circulating VCAM-1 in patients with DCM [23,24]. Thus, IL-13 may contribute to angiogenic activity by the induction of VCAM-1 in DCM.…”

Section: Discussionmentioning

confidence: 99%

Serum markers of angiogenesis and myocardial ultrasonic tissue characterization in patients with dilated cardiomyopathy

Ohtsuka

Inoue

Hara

et al. 2005

European J of Heart Fail

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Background and aims: It has been proven that a disturbance in angiogenesis contributes to the progression of myocardial interstitial fibrosis in idiopathic dilated cardiomyopathy (DCM). This study was designed to evaluate the relationship between serum activity of angiogenic factors and myocardial ultrasonic tissue characterization in patients with DCM. Methods and results:We studied 30 patients with DCM and 15 healthy control subjects. Serum levels of vascular endothelial growth factor (VEGF), interleukin (IL)-4 and IL-13 were measured using enzyme-linked immunosorbent assay. We determined calibrated myocardial integrated backscatter (IB) as the value of myocardial interstitial fibrosis using ultrasonic tissue characterization and also quantified the magnitude of cyclic variations in IB (CV-IB). Serum levels of VEGF and IL-13 were significantly higher in patients with DCM than in control subjects (both Pb0.05). Calibrated IB was significantly higher and CV-IB was markedly lower in patients with DCM than in control subjects (both Pb0.01). In patients with DCM, the levels of IL-13 significantly correlated with calibrated IB (r=0.520, P=0.018). In addition, there was a significant negative correlation between levels of VEGF and CV-IB (r=À0.611, P=0.007). Conclusion: The increase in serum VEGF and IL-13 may be closely related to alterations in myocardial texture in DCM.

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Increased plasma adhesion molecule levels in patients with heart failure who have ischemic heart disease and dilated cardiomyopathy

Cited by 38 publications

References 28 publications

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

The role of vascular cell adhesion molecule 1/ very late activation antigen 4 in endothelial progenitor cell recruitment to rheumatoid arthritis synovium

Conflicting effects of nitric oxide and oxidative stress in chronic heart failure: potential therapeutic strategies

Serum markers of angiogenesis and myocardial ultrasonic tissue characterization in patients with dilated cardiomyopathy

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