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Titolo:
DECREASED BLOOD-FLOW RATE DISRUPTS ENDOTHELIAL REPAIR IN-VIVO
Autore:
VYALOV S; LANGILLE BL; GOTLIEB AI;
Indirizzi:
TORONTO GEN HOSP,RES INST,VASC RES LAB,BANTING & BEST DIABET CTR,200 ELIZABETH ST,CCRW 1-857 TORONTO ON M5G 2C4 CANADA TORONTO GEN HOSP,RES INST,VASC RES LAB,BANTING & BEST DIABET CTR TORONTO ON M5G 2C4 CANADA UNIV TORONTO,DEPT PATHOL TORONTO ON CANADA UNIV TORONTO,CARDIOVASC RES CTR TORONTO ON CANADA
Titolo Testata:
The American journal of pathology
fascicolo: 6, volume: 149, anno: 1996,
pagine: 2107 - 2118
SICI:
0002-9440(1996)149:6<2107:DBRDER>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; MICROTUBULE-ORGANIZING CENTERS; SMOOTH-MUSCLE CELLS; SHEAR-STRESS; AORTIC ENDOTHELIUM; INVITRO REENDOTHELIALIZATION; CENTROSOME REDISTRIBUTION; MICROFILAMENT BUNDLES; ARTERIAL INJURY; F-ACTIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
48
Recensione:
Indirizzi per estratti:
Citazione:
S. Vyalov et al., "DECREASED BLOOD-FLOW RATE DISRUPTS ENDOTHELIAL REPAIR IN-VIVO", The American journal of pathology, 149(6), 1996, pp. 2107-2118

Abstract

Both local hemodynamics and endothelial injury have been implicated in vascular disorders including bypass graft failure and atherogenesis,but little is known about the effect of local blood flow conditions on repair of endothelial injury. We decreased blood flow rates and shear stresses in common carotid arteries of rabbits by ligating the ipsilateral external carotid artery. After 24 hours, endothelial cells wereless elongated, contained fewer central microfilament bundles, and showed less polarity of the centrosome toward the heart than endothelialcells in unmanipulated carotid arteries. To examine wound repair, we made narrow longitudinal intimal wounds at the time of flow reduction using a nylon monofilament device. In arteries with normal blood flows, endothelial cells at the edge of the wound initially spread and elongated in the direction of the wound. The dense peripheral band of actin was attenuated and central micro-filaments became more prominent. Endothelial cells remained in close contact with their neighbors in the monolayer. The centrosome of cells adjacent to the wound was redistributed toward the wound side of the nucleus at 6 and 12 hours. Complete closure occurred by 24 hours, at which time the elongated endothelial cells covering the wound were organized in a herringbone pattern with their downstream ends at the center of the wound. With decreased flow and shear stress, the cells at the wound edge spread less than those in normal vessels at 12 hours after wounding and were randomly orientedand polygonal in shape. Also, re-endothelialization proceeded more slowly and there was a marked reduction of central microfilaments in cells at the wound edge. At 24 hours, the wounds were still open, the endothelial cells covering the central portion of the wound did not maintain intimate contact with their neighbors, and orientation of the centrosome toward the wound was reduced. We hypothesize that loss of cell-cell contact during repair at low flow rates and low shear stress disrupts intercellular communication and results in disruption of cytoskeletal reorganization during repair, thereby slowing the repair process.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 05:33:39