Resistance to Apoptosis in Smooth Muscle Cells and Stent-Induced Stenosis in Coronary and Peripheral Arteries
type: CreativeWork
description: Occlusive vascular disease is one of the major causes of morbidity and mortality in the United States. Treatment often involves angioplasty and stenting. In 30-50% of angioplasty cases, success is limited by re-narrowing (restenosis) of the artery. Stenting offers the advantage of a slightly lower restenosis rate. However, this rate is still significant. Studies aimed at further understanding the restenotic disease process and the cells that contribute to it would aid in the development of treatment options. The restenotic process involves the proliferation, apoptosis and migration of vascular smooth muscle cells (VSMCs). Apoptosis has been shown to be an integral part of lesion development in atherosclerosis and restenosis after angioplasty. Subsequently, alterations in this process could significantly affect and determine the extent of lesion development. It was hypothesized that arteries from alternate embryological origins react differently with regards to the development of in-stent stenosis and that vascular smooth muscle cells derived from different arteries are unique with regards to their apoptotic responses. To test these hypotheses, in vivo studies were performed comparing central and peripheral arteries in a swine model of stenting and in vitro studies were done looking at apoptotic responses of human coronary and aortic VSMCs. Swine studies of stenosis after stenting demonstrated a significantly higher level of intimal area development in coronary arteries compared to the peripheral internal iliac arteries. There was an increase in percent lumen stenosis and maximal intimal thickness; however, these differences did not reach statistical significance. Utilizing in vitro studies on VSMCs, celis derived from human coronary arteries demonstrated a higher level of resistance to staurosporine-induced apoptosis than human aortic VSMCs. This observation was confirmed using calphostin C mediated VSMC apoptosis. IGF-1, an anti-apoptotic growth factor for VSMCs, w…
abstract: Occlusive vascular disease is one of the major causes of morbidity and mortality in the United States. Treatment often involves angioplasty and stenting. In 30-50% of angioplasty cases, success is limited by re-narrowing (restenosis) of the artery. Stenting offers the advantage of a slightly lower restenosis rate. However, this rate is still significant. Studies aimed at further understanding the restenotic disease process and the cells that contribute to it would aid in the development of treatment options. The restenotic process involves the proliferation, apoptosis and migration of vascular smooth muscle cells (VSMCs). Apoptosis has been shown to be an integral part of lesion development in atherosclerosis and restenosis after angioplasty. Subsequently, alterations in this process could significantly affect and determine the extent of lesion development. It was hypothesized that arteries from alternate embryological origins react differently with regards to the development of in-stent stenosis and that vascular smooth muscle cells derived from different arteries are unique with regards to their apoptotic responses. To test these hypotheses, in vivo studies were performed comparing central and peripheral arteries in a swine model of stenting and in vitro studies were done looking at apoptotic responses of human coronary and aortic VSMCs. Swine studies of stenosis after stenting demonstrated a significantly higher level of intimal area development in coronary arteries compared to the peripheral internal iliac arteries. There was an increase in percent lumen stenosis and maximal intimal thickness; however, these differences did not reach statistical significance. Utilizing in vitro studies on VSMCs, celis derived from human coronary arteries demonstrated a higher level of resistance to staurosporine-induced apoptosis than human aortic VSMCs. This observation was confirmed using calphostin C mediated VSMC apoptosis. IGF-1, an anti-apoptotic growth factor for VSMCs, w…
author: Krueger, Kristopher Daniel
language: en_US
date published: 2003-02-07
date modified: 2026-07-24T01:50:24Z
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/10504/68516