The role of endothelial cell adhesion molecules in the development of atherosclerosis

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The vascular endothelium serves as a dynamic interface between circulating blood elements and the interstitial tissues. As such, it communicates to cells within the vessel wall as well as to the surrounding tissue, sensing its environment and responding accordingly. The vasculature must maintain a delicate balance when initiating a functional response by producing both proinflammatory and antiinflammatory mediators, vasoconstrictors and vasodilators, growth stimulators and inhibitors, and prothrombogenic and antithrombogenic factors. Any response to injurious agents could lead to pathology. Confounding this complex interplay is the fact that the very response to injury that may have developed to undo the damage may itself be even more deleterious. One response to injury by the endothelium is the new or increased expression of surface receptors for immune elements. In atherosclerosis, the adhesion of monocytes (and T cells) to the endothelium is a key event triggered by some form of insult. Subsequent events include monocytic infiltration of the vessel wall, alterations in lipid metabolism, and the activation of these cells into foam cells. The presence of large numbers of foam cells in the intima may produce a high concentration of cytokines and growth factors within a localized area, extracellular matrix perturbations, smooth muscle cell proliferation, and ultimately platelet aggregation at the site of stenosis. Endothelial cells themselves will not only elaborate factors after the initial injury to the vessel wall but also in response to the factors produced by foam cells within the plaque. These endothelial cell factors include MCP-1, a chemoattractant for monocytes (179,180), IL-1 (63,64), IL-6 (interleukin-6) (65-67), IL-8 (interleukin 8) (181), and PDGF, a potent smooth muscle mitogen (4,72) (Fig. 3). Endothelial cells will propagate an inflammatory response long after the initial insult to the arterial vessel. A chronic cycle of endothelial cell activation and leukocyte infiltration is constitutively activated. Thus, all of the cellular elements of the vessel wall, as well as the atherosclerotic plaque itself, elaborate cytokines and growth factors that amplify and propagate the pathological process.

Original languageEnglish (US)
Pages (from-to)17-28
Number of pages12
JournalCardiovascular Pathology
Volume1
Issue number1
DOIs
StatePublished - 1992

Fingerprint

Cell Adhesion Molecules
Foam Cells
Atherosclerosis
Endothelial Cells
Interleukin-6
Endothelium
Monocytes
Intercellular Signaling Peptides and Proteins
Wounds and Injuries
Cytokines
Growth Inhibitors
Chemotactic Factors
Vascular Endothelium
Vasoconstrictor Agents
Atherosclerotic Plaques
Pathologic Processes
Interleukin-8
Vasodilator Agents
Interleukin-1
Platelet Aggregation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pathology and Forensic Medicine

Cite this

@article{7a0c2eedc03d4a5691bfe2ebe52a0240,
title = "The role of endothelial cell adhesion molecules in the development of atherosclerosis",
abstract = "The vascular endothelium serves as a dynamic interface between circulating blood elements and the interstitial tissues. As such, it communicates to cells within the vessel wall as well as to the surrounding tissue, sensing its environment and responding accordingly. The vasculature must maintain a delicate balance when initiating a functional response by producing both proinflammatory and antiinflammatory mediators, vasoconstrictors and vasodilators, growth stimulators and inhibitors, and prothrombogenic and antithrombogenic factors. Any response to injurious agents could lead to pathology. Confounding this complex interplay is the fact that the very response to injury that may have developed to undo the damage may itself be even more deleterious. One response to injury by the endothelium is the new or increased expression of surface receptors for immune elements. In atherosclerosis, the adhesion of monocytes (and T cells) to the endothelium is a key event triggered by some form of insult. Subsequent events include monocytic infiltration of the vessel wall, alterations in lipid metabolism, and the activation of these cells into foam cells. The presence of large numbers of foam cells in the intima may produce a high concentration of cytokines and growth factors within a localized area, extracellular matrix perturbations, smooth muscle cell proliferation, and ultimately platelet aggregation at the site of stenosis. Endothelial cells themselves will not only elaborate factors after the initial injury to the vessel wall but also in response to the factors produced by foam cells within the plaque. These endothelial cell factors include MCP-1, a chemoattractant for monocytes (179,180), IL-1 (63,64), IL-6 (interleukin-6) (65-67), IL-8 (interleukin 8) (181), and PDGF, a potent smooth muscle mitogen (4,72) (Fig. 3). Endothelial cells will propagate an inflammatory response long after the initial insult to the arterial vessel. A chronic cycle of endothelial cell activation and leukocyte infiltration is constitutively activated. Thus, all of the cellular elements of the vessel wall, as well as the atherosclerotic plaque itself, elaborate cytokines and growth factors that amplify and propagate the pathological process.",
author = "Berman, {Joan W.} and Calderon, {Tina M.}",
year = "1992",
doi = "10.1016/1054-8807(92)90005-9",
language = "English (US)",
volume = "1",
pages = "17--28",
journal = "Cardiovascular Pathology",
issn = "1054-8807",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - The role of endothelial cell adhesion molecules in the development of atherosclerosis

AU - Berman, Joan W.

AU - Calderon, Tina M.

PY - 1992

Y1 - 1992

N2 - The vascular endothelium serves as a dynamic interface between circulating blood elements and the interstitial tissues. As such, it communicates to cells within the vessel wall as well as to the surrounding tissue, sensing its environment and responding accordingly. The vasculature must maintain a delicate balance when initiating a functional response by producing both proinflammatory and antiinflammatory mediators, vasoconstrictors and vasodilators, growth stimulators and inhibitors, and prothrombogenic and antithrombogenic factors. Any response to injurious agents could lead to pathology. Confounding this complex interplay is the fact that the very response to injury that may have developed to undo the damage may itself be even more deleterious. One response to injury by the endothelium is the new or increased expression of surface receptors for immune elements. In atherosclerosis, the adhesion of monocytes (and T cells) to the endothelium is a key event triggered by some form of insult. Subsequent events include monocytic infiltration of the vessel wall, alterations in lipid metabolism, and the activation of these cells into foam cells. The presence of large numbers of foam cells in the intima may produce a high concentration of cytokines and growth factors within a localized area, extracellular matrix perturbations, smooth muscle cell proliferation, and ultimately platelet aggregation at the site of stenosis. Endothelial cells themselves will not only elaborate factors after the initial injury to the vessel wall but also in response to the factors produced by foam cells within the plaque. These endothelial cell factors include MCP-1, a chemoattractant for monocytes (179,180), IL-1 (63,64), IL-6 (interleukin-6) (65-67), IL-8 (interleukin 8) (181), and PDGF, a potent smooth muscle mitogen (4,72) (Fig. 3). Endothelial cells will propagate an inflammatory response long after the initial insult to the arterial vessel. A chronic cycle of endothelial cell activation and leukocyte infiltration is constitutively activated. Thus, all of the cellular elements of the vessel wall, as well as the atherosclerotic plaque itself, elaborate cytokines and growth factors that amplify and propagate the pathological process.

AB - The vascular endothelium serves as a dynamic interface between circulating blood elements and the interstitial tissues. As such, it communicates to cells within the vessel wall as well as to the surrounding tissue, sensing its environment and responding accordingly. The vasculature must maintain a delicate balance when initiating a functional response by producing both proinflammatory and antiinflammatory mediators, vasoconstrictors and vasodilators, growth stimulators and inhibitors, and prothrombogenic and antithrombogenic factors. Any response to injurious agents could lead to pathology. Confounding this complex interplay is the fact that the very response to injury that may have developed to undo the damage may itself be even more deleterious. One response to injury by the endothelium is the new or increased expression of surface receptors for immune elements. In atherosclerosis, the adhesion of monocytes (and T cells) to the endothelium is a key event triggered by some form of insult. Subsequent events include monocytic infiltration of the vessel wall, alterations in lipid metabolism, and the activation of these cells into foam cells. The presence of large numbers of foam cells in the intima may produce a high concentration of cytokines and growth factors within a localized area, extracellular matrix perturbations, smooth muscle cell proliferation, and ultimately platelet aggregation at the site of stenosis. Endothelial cells themselves will not only elaborate factors after the initial injury to the vessel wall but also in response to the factors produced by foam cells within the plaque. These endothelial cell factors include MCP-1, a chemoattractant for monocytes (179,180), IL-1 (63,64), IL-6 (interleukin-6) (65-67), IL-8 (interleukin 8) (181), and PDGF, a potent smooth muscle mitogen (4,72) (Fig. 3). Endothelial cells will propagate an inflammatory response long after the initial insult to the arterial vessel. A chronic cycle of endothelial cell activation and leukocyte infiltration is constitutively activated. Thus, all of the cellular elements of the vessel wall, as well as the atherosclerotic plaque itself, elaborate cytokines and growth factors that amplify and propagate the pathological process.

UR - http://www.scopus.com/inward/record.url?scp=0002794720&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0002794720&partnerID=8YFLogxK

U2 - 10.1016/1054-8807(92)90005-9

DO - 10.1016/1054-8807(92)90005-9

M3 - Article

AN - SCOPUS:0002794720

VL - 1

SP - 17

EP - 28

JO - Cardiovascular Pathology

JF - Cardiovascular Pathology

SN - 1054-8807

IS - 1

ER -