Selective Interference Targeting of Lnk in Umbilical Cord-Derived Late Endothelial Progenitor Cells Improves Vascular Repair, Following Hind Limb Ischemic Injury, via Regulation of JAK2/STAT3 Signaling

Stem Cells ◽  
2015 ◽  
Vol 33 (5) ◽  
pp. 1490-1500 ◽  
Author(s):  
Sang Hun Lee ◽  
Kyeung Bin Lee ◽  
Jun Hee Lee ◽  
Songhwa Kang ◽  
Hwi Gon Kim ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Umbilical Cord ◽  
Hind Limb ◽  
Ischemic Injury ◽  
Vascular Repair ◽  
Endothelial Progenitor ◽  
Stat3 Signaling ◽  
Selective Interference

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.

Identification of functional endothelial progenitor cells suitable for the treatment of ischemic tissue using human umbilical cord blood

Blood ◽  
2007 ◽  
Vol 110 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Masumi Nagano ◽  
Toshiharu Yamashita ◽  
Hiromi Hamada ◽  
Kinuko Ohneda ◽  
Ken-ichi Kimura ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cord Blood ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Human Umbilical Cord ◽  
Aldh Activity ◽  
Endothelial Progenitor ◽  
Hematopoietic Stem

Umbilical cord blood (UCB) has been used as a potential source of various kinds of stem cells, including hematopoietic stem cells, mesenchymal stem cells, and endothelial progenitor cells (EPCs), for a variety of cell therapies. Recently, EPCs were introduced for restoring vascularization in ischemic tissues. An appropriate procedure for isolating EPCs from UCB is a key issue for improving therapeutic efficacy and eliminating the unexpected expansion of nonessential cells. Here we report a novel method for isolating EPCs from UCB by a combination of negative immunoselection and cell culture techniques. In addition, we divided EPCs into 2 subpopulations according to the aldehyde dehydrogenase (ALDH) activity. We found that EPCs with low ALDH activity (Alde-Low) possess a greater ability to proliferate and migrate compared to those with high ALDH activity (Alde-High). Moreover, hypoxia-inducible factor proteins are up-regulated and VEGF, CXCR4, and GLUT-1 mRNAs are increased in Alde-Low EPCs under hypoxic conditions, while the response was not significant in Alde-High EPCs. In fact, the introduction of Alde-Low EPCs significantly reduced tissue damage in ischemia in a mouse flap model. Thus, the introduction of Alde-Low EPCs may be a potential strategy for inducing rapid neovascularization and subsequent regeneration of ischemic tissues.

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