Regulatory Mechanisms Underlying the Differentiation of Mesenchymal Stem Cells to Endothelial Cells
type: CreativeWork
description: Cardiovascular disease is the foremost cause of mortality in the United States. Myocardial infarction often results from atherosclerotic occlusion of coronary arteries. Coronary angioplasty is performed to restore cardiac blood flow and function. Angioplasty is the most widely used interventional technique for coronary occlusion events. However, long term benefits are curtailed by vascular endothelium injury. Endothelial denudation often leads to the processes of thrombosis, inflammation, and restenosis that subject patients to reoccurrence of myocardial infarction. The current clinical therapies prescribed to patients with coronary artery disease are a combination of drugs used to control blood pressure, lipid levels and glucose levels. Unfortunately, none of these treatment regimens are designed to repair or replace damaged endothelium. |Bone marrow (BM)-derived mesenchymal stem cells (MSCs) can differentiate into endothelial cells (ECs) in the presence of vascular endothelial growth factor (VEGF) — 165 in vitro. Translational models have demonstrated that differentiated BM-derived MSCs can be transplanted into the site of angioplasty-induced endothelial injury. However, re-endothelialization by VEGF-induced BM-derived MSCs remains a complex clinical challenge. Following intracoronary or transendocardial delivery of the BM-derived MSCs, only ~10% of the differentiating cells engraft, and the majority of those persist as immature ECs. Currently, the mechanisms underlying EC-engraftment and re-endothelialization are not well understood. In patients undergoing coronary intervention, the mechanical process involved in performing angioplasty itself is known to stimulate atherogenesis. The goal of this study is to decipher a potential role of angioplasty-induced atherogenic mediators on the differentiation of BM-derived MSCs into ECs. The central hypothesis of these studies is that pro-atherogenic mediators, which are triggered after an angioplasty, inhibit VEGF-165-ind…
abstract: Cardiovascular disease is the foremost cause of mortality in the United States. Myocardial infarction often results from atherosclerotic occlusion of coronary arteries. Coronary angioplasty is performed to restore cardiac blood flow and function. Angioplasty is the most widely used interventional technique for coronary occlusion events. However, long term benefits are curtailed by vascular endothelium injury. Endothelial denudation often leads to the processes of thrombosis, inflammation, and restenosis that subject patients to reoccurrence of myocardial infarction. The current clinical therapies prescribed to patients with coronary artery disease are a combination of drugs used to control blood pressure, lipid levels and glucose levels. Unfortunately, none of these treatment regimens are designed to repair or replace damaged endothelium. |Bone marrow (BM)-derived mesenchymal stem cells (MSCs) can differentiate into endothelial cells (ECs) in the presence of vascular endothelial growth factor (VEGF) — 165 in vitro. Translational models have demonstrated that differentiated BM-derived MSCs can be transplanted into the site of angioplasty-induced endothelial injury. However, re-endothelialization by VEGF-induced BM-derived MSCs remains a complex clinical challenge. Following intracoronary or transendocardial delivery of the BM-derived MSCs, only ~10% of the differentiating cells engraft, and the majority of those persist as immature ECs. Currently, the mechanisms underlying EC-engraftment and re-endothelialization are not well understood. In patients undergoing coronary intervention, the mechanical process involved in performing angioplasty itself is known to stimulate atherogenesis. The goal of this study is to decipher a potential role of angioplasty-induced atherogenic mediators on the differentiation of BM-derived MSCs into ECs. The central hypothesis of these studies is that pro-atherogenic mediators, which are triggered after an angioplasty, inhibit VEGF-165-ind…
author: Ikhapoh, Izuagie P. A.
language: en_US
date published: 2016-08-10
date modified: 2026-07-24T01:50:02Z
provider: Creighton University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Creighton University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10504/90238