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Cited by 114Atherosclerosis and Cardiovascular DiseasesReceptor Mechanisms and SignalingBlood Coagulation and Thrombosis Mechanisms

Vascular transcellular signaling.

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Marcus, Aaron J., Hajjar, David P.·1993·Journal of Lipid Research
DOI 10.1016/s0022-2275(20)35344-x
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Abstract

Receptors on the cell surface are targets for ligands that tor was widely expressed in human atheroma.It was direct cell-cell interactions.Receptors can detect a variety identified in macrophage-rich areas and in locations rich of signal molecules such as catecholamines, cytokines, in vascular smooth muscle cells.Thus, activation of the neurotransmitters, and eicosanoids.Ligand binding initi-thrombin receptor may contribute to fibrosis and the ates, intracellular signaling processes and a cascade of bi-inflammatory reaction occurring in the vasculature durochemical events that induce changes in the cell.A cur-ing development of atherosclerosis and also in the restenorent fundamental problem is to define the mechanisms sis complicating surgical bypass procedures (1).It is now involved in the regulation of transmembrane signaling evident that atherosclerosis and thrombosis are parallel processes, how they achieve specificity, and how dysregu-events that must be studied together in order to comprelation may influence disease.TW such diseases that appear hend basic aspects of pathology and develop therapeutic linked with one another and share many common alterations modalities (2-6).in metabolic events are atherosclerosis and thrombosis.In discussing the novel, "Madame Bovary," Vladimir Atherosclerosis may be defined as a progressive disease Nabokov stated the following: "Three forces make and process involving large to medium-sized muscular and mold a human being: heredity, environment and the large elastic arteries.The advanced lesion consists of unknown agent X.Of these the second, environment, is elevated focal intimal plaques with a necrotic central core by far the least important, while the last, agent X, is by containing lysed cells, cholesteryl ester crystals, lipid-far the most influential.In the case of characters living in laden foam cells, and plasma proteins such as fibrino-books, it is of course the author who controls, directs and gedfibrin.Overlying the central core is a cellular zone applies the three forces."(7).These statements are very containing smooth muscle cells, macrophages, and Tapplicable to the problem at hand.Consider myocardial lymphocytes.The lesion is capped superficially by fibrous infarction: heredity does come into play if we actissue.Vascularization of peripheral areas of the plaque is knowledge a positive family history, hypertension, diaoften observed.These fibro-fatty plaques are found in the betes, and a cholesterol over 200 mg/dl.We could also add abdominal aorta, coronary and internal carotid arteries, elevated LDL and reduced HDL levels.Elevations of and other critical areas of the vasculature.The presence Lp[a] comprise another possibly inherited risk factor for of atheroma renders the patient thrombosis-prone, coronary artery disease.Environment would include presumably because the plaques gradually enter a compli-cigarette smoking and probably obesity.However, in the cated phase when they become calcified, fissured, or ulcerated.The latter surfaces act as powerful agonists for platelet activation, and recruitment and thrombus forma-~ ;ion.Fifty percent of deaths in the United States are at-Abbreviations: LDL, low density lipoproteins; HDL, high density tributable to complications of atherosclerosis; of these ~roxidopmta~5,13~di~noic acid (pmtaglandin G 2 ) endoperoxide; lipoproteins; Lp[a], lipoprotein(a]; PGG?, 15-hydroperoxy-9a,lla-50% are directly due to coronary thrombosis with conse-~c H ~, 15-hydroxy-~,lla-perauidoapnma-5.13-dienoicacid (prostaglandin quent myocardial infarction.H,) endoperoxide; 12-HETE, (12S)-hydroxy-5.8-~,lO-~m~,l4-cireicosatetraenoicacid; ATP, adenosine triphosphate; 12.20-diHETE.including growth factors, are the inciting events for the PGDF, platelet-derived growth factor; FGF, fibroblast growth factor;'latelet adherence9 activation, and re1ease Of agonists912S,20-dihydroxy-5,8,]0,14-cicosatet~a~n~ic acid; CE, &olesteryl ester;predisposition to thrombosis-an event that accompanies IL-I, interleukin-1; Z F , transforming growth factor.TNF, tumor necrosis factor, IFN, interferon; GM-CSF, granulocyte-monocytesis.Further evidence in support of the thrombosis compooncogene derived from the avian myeloblastosis virus (AMV); c-sir, nent concept has recently been provided.In a study of ex-pmto-oncogcnc derived from simian Sarcoma Virus (ssv); HMG-Cd?pression of the thrombin receptor in arterial tissue by in ase; DAG, diacylglFerol.hydroxymethylglutaryl-CoA; ACAT, acyl-CoA: cholesterol acyltransfersitu hybridization and immunohistochemistry, this recep-'To whom correspondence and reprint requests should be addresscd.and defines the terminal stage of untnwed athemsclero-co~ony-stimu~ating factor, acyl-c&, acyl c*nzyme A; c -v c , proto-

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  1. Krone, W., P. Kaczmarczyk, D. Muller-Wieland, and H. Greten. 1985. The prostacyclin analog iloprost and prostaglandin El sup- press sterol synthesis in freshly isolated human mononuclear leuko- cytes. Biochim. Biophys. Acta. 835: 154-157.

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Authors
Marcus, A. J., & Hajjar, D. P.
Affiliations
  • Veterans Health Administration (US)
  • Cornell University (US)
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
1993-12
Volume
34
Issue
12
Pages
2017-2031
ISSN
0022-2275 (ISSN-L)
DOI
10.1016/s0022-2275(20)35344-x
OpenAlex
W2186205091
Cited by
114
References
105
Citations by year
2021: 1 · 2020: 2 · 2017: 2 · 2016: 3 · 2015: 5 · 2014: 2 · 2012: 4
FWCI
3.53
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Lipid Research (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (5r01hl039701-02, 5r01hl049666-09)
  • National Heart, Lung, and Blood Institute (P01HL046403, HL-39701, HL49666, HL-46403)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Keywords
atherosclerosis, thrombosis, vascular smooth muscle cells, macrophages, cell-cell interactions, protease-activated receptor 1, restenosis, foam cells, vascular inflammation, cytokines, eicosanoids, catecholamines, plaque fibrosis, atherosclerotic plaque
MeSH terms
Arteriosclerosis, Blood Vessels, Cell Communication, Humans, Thrombosis, Signal Transduction, Eicosanoids, Cytokines

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