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Titolo:
Activation of vascular endothelial cell adhesion molecule expression by sickle blood cells
Autore:
Brown, MD; Wick, TM; Eckman, JR;
Indirizzi:
Emory Univ, Sch Med, Div Hematol & Oncol, Atlanta, GA 30303 USA Emory Univ Atlanta GA USA 30303 iv Hematol & Oncol, Atlanta, GA 30303 USA Georgia Inst Technol, Sch Chem Engn, Atlanta, GA 30332 USA Georgia Inst Technol Atlanta GA USA 30332 hem Engn, Atlanta, GA 30332 USA Grady Mem Hosp, Georiga NIH Sickle Cell Ctr, Atlanta, GA USA Grady Mem Hosp Atlanta GA USA origa NIH Sickle Cell Ctr, Atlanta, GA USA
Titolo Testata:
PEDIATRIC PATHOLOGY & MOLECULAR MEDICINE
fascicolo: 1, volume: 20, anno: 2001,
pagine: 47 - 72
SICI:
1522-7952(200101)20:1<47:AOVECA>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; ERYTHROCYTE ADHERENCE; CEREBROVASCULAR ACCIDENTS; CIRCULATING CYTOKINES; CEREBRAL INFARCTION; TRANSFUSION THERAPY; CONTROLLED FLOW; LARGE-VESSEL; RISK-FACTORS; DISEASE;
Keywords:
cell adhesion molecules; E-selectin; endothelial activities; endothelial adhesion; ICAM-1; inflammation; interleukin-1; leukocytes; sickle cell anemia; TNF-alpha VCAM-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Eckman, JR Emory Univ, Sch Med, Div Hematol & Oncol, 69 Butler St SE, Atlanta, GA 30303 USA Emory Univ 69 Butler St SE Atlanta GA USA 30303 a, GA 30303 USA
Citazione:
M.D. Brown et al., "Activation of vascular endothelial cell adhesion molecule expression by sickle blood cells", PEDIAT PATH, 20(1), 2001, pp. 47-72

Abstract

Microvascular complications in sickle cell disease occur as a result of obstruction of small vessels Microvascular by deoxygenated sickle cells. Cerebrovascular complications are also common and result from obstruction of large blood vessels by thrombosis with changes in vessels that have some similarity to those found in arteriosclerotic vascular disease. Endothelial damage and activation from sickle cell-endothelial interactions may contributeto both. We find that endothelial cells have increased expression of VCAM-1, E-selectin, and ICAM-1 when exposed to sickle blood cells. The concentration-dependent, sickle-induced, adhesion molecule expression is significantly greater than that promoted by normal cells. The time course of Cell Adhesion Molecule ( CAM) expression is similar to that induced by TNF-alpha and IL1. Studies after white cell enrichment and reduction suggest leukocytes are the primary mediators. CAM expression by endothelial cells appears stimulated bysoluble factors. Antibody inhibition studies support TNF-alpha and IL-1, produced by sickle leukocytes, as the primary soluble factors responsible for the observed CAM expression. Both the induction of endothelial CAM expression and subsequent endothelial adherence of sickle erythrocytes may play significant roles in the pathophysiology of sickle-related complications, and reduction in CAM expression may provide a new approach to treatment.

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Documento generato il 18/01/20 alle ore 07:32:53