scholarly journals The importance of the functional network between endothelial microparticles and late endothelial progenitor cells for understanding the physiological aspects of this new vascular repair system

2017 ◽  
Vol 222 (1) ◽  
pp. e12931 ◽  
Author(s):  
R. A. Condorelli ◽  
A. E. Calogero ◽  
S. La Vignera
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Functional Network ◽  
Repair System ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Endothelial Microparticles

Intrinsic Vascular Repair by Endothelial Progenitor Cells in Acute Coronary Syndromes: an Update Overview

2018 ◽  
Vol 15 (1) ◽  
pp. 35-47 ◽  
Author(s):  
Vânia Leal ◽  
Carlos Fontes Ribeiro ◽  
Bárbara Oliveiros ◽  
Natália António ◽  
Sónia Silva
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Acute Coronary Syndromes ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Coronary Syndromes

Endothelial Progenitor Cells for Vascular Repair

2010 ◽  
pp. 297-320
Author(s):  
Melissa A. Brown ◽  
Cindy S. Cheng ◽  
George A. Truskey
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Repair ◽  
Endothelial Progenitor

Effects of insulin resistance on endothelial progenitor cells and vascular repair

2009 ◽  
Vol 117 (5) ◽  
pp. 173-190 ◽  
Author(s):  
Richard M. Cubbon ◽  
Matthew B. Kahn ◽  
Stephen B. Wheatcroft
Keyword(s):  
Insulin Resistance ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Damage ◽  
Glucose Disposal ◽  
No Production ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
The Metabolic Syndrome ◽  
Underlying Mechanisms

Insulin resistance, a key feature of obesity, the metabolic syndrome and Type 2 diabetes mellitus, results in an array of metabolic and vascular phenomena which ultimately promote the development of atherosclerosis. Endothelial dysfunction is intricately related to insulin resistance through the parallel stimulatory effects of insulin on glucose disposal in metabolic tissues and NO production in the endothelium. Perturbations characteristic of insulin resistance, including dyslipidaemia, inflammation and oxidative stress, may jeopardize the structural or functional integrity of the endothelium. Recent evidence suggests that endothelial damage is mitigated by endogenous reparative processes which mediate endothelial regeneration. EPCs (endothelial progenitor cells) are circulating cells which have been identified as mediators of endothelial repair. Several of the abnormalities associated with insulin resistance, including reduced NO bioavailability, increased production of ROS (reactive oxygen species) and down-regulation of intracellular signalling pathways, have the potential to disrupt EPC function. Improvement in the number and function of EPCs may contribute to the protective actions of evidence-based therapies to reduce cardiometabolic risk. In the present article, we review the putative effects of insulin resistance on EPCs, discuss the underlying mechanisms and highlight potential therapeutic manoeuvres which could improve vascular repair in individuals with insulin resistance.

Association of Endothelial Microparticles (EMP) and Endothelial Progenitors with Serum Cholesterol Levels.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1819-1819
Author(s):  
Joaquin J. Jimenez ◽  
Alexander Ferreira ◽  
Hannah J. Dodson ◽  
Katherine M. Lens ◽  
Lucia M. Mauro ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Colony Formation ◽  
Vascular Endothelial Cell ◽  
Endothelial Progenitor ◽  
Endothelial Microparticles ◽  
Cholesterol Levels ◽  
Circulating Endothelial Progenitor Cells

Abstract INTRODUCTION: High cholesterol (HC) is known to adversely affect endothelial cells (EC) and has been shown to correlate with decreased levels of circulating endothelial progenitor cells (CEPC). We assayed endothelial microparticles (EMP), a sensitive indicator of EC perturbation, to investigate relations among HC, CEPC, and injury of coronary artery endothelial cells (CAEC), both in vivo and in vitro. METHODS: Twelve subjects with normal cholesterol (150 ±30 mg/dL, control) and 12 with HC (250 ±25) were studied. EMP were assayed by flow cytometry using fluorescent antibodies and CAEC were cultured as previously described [Jimenez et al, Thromb Res 109:175, 2003]. CEPC were isolated, cultured, and assayed for endothelial colony formation (CFU) as described [Hill et al, NEJM 348:593, 2003]. RESULTS: Comparing the two groups, EMP measured by CD31+/CD42b− were nearly 2.5-fold elevated in HC as compared to controls (1.7 ±0.5 ×106/mL vs.0.35 ±0.02 ×106/mL; p<0.01). Cholesterol levels correlated well with this measure of EMP (R=0.60, p=0.002). However, no significant correlation was found between CD62E+ EMP and cholesterol levels. Assay of CEPC revealed a nearly 2.5-fold decrease in CFU in HC vs. controls (10 ±2 vs. 25 ±4; p<0.01). In studies in vitro, CEPC from controls were cultured in presence of 20% 0.1μm filtered plasma from members of both groups. The HC group plasma inhibited CEPC colony formation by almost 50% (23 ±3.5 CFU for control plasma vs. 13 ±4 colonies for HC plasma). We next assessed the longer-term effect of HC plasma on CAEC cultures. Six-day culture of CAEC in the presence of 20% plasma resulted in a significant increase of CD31+/CD42b− EMP from CAEC treated with HC plasma vs. normal plasma (6.5 ±0.7 ×106/mL vs. 0.23 ±0.03 ×106/mL; p=0.02). CONCLUSION: These results suggest that EMP are useful markers to monitor cholesterol mediated-EC changes. High EMP levels inversely reflect the vascular endothelial cell regeneration potential due to decreased circulating endothelial progenitor cells.

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