Document Detail

Endothelial wounds with disruption in cell migration repair primarily by cell proliferation.
MedLine Citation:
PMID:  7731397     Owner:  NLM     Status:  MEDLINE    
Disruption of vascular integrity results in activation of endothelial cells to initiate repair. Cytoskeletal reorganization, cell spreading, migration, and proliferation are important processes which regulate rapid and efficient repair. Cell proliferation has been thought to be a secondary event and dependent to a large extent on prior cell migration. We used a model of dysfunctional repair to test the hypothesis that a reduction in migration will result in a reduction in cell proliferation. The extent of cell proliferation was studied in an in vitro repair model, in which endothelial function is studied during the closure of a 1500-microns mechanically induced wound in a confluent monolayer. Dysfunctional repair is induced in this model by transiently inhibiting endothelial cell transcription. Wounds are incubated with actinomycin D at the time of wounding for 2 hr, which results in wound closure taking about 4.5 times longer than normal. Cell proliferation is measured by 5-bromo-2'-deoxyuridine incorporation. In actinomycin D-treated wounds, the rate of cell migration is reduced, and for the first 120 hr very little cell proliferation occurs and it involves the first 4 rows of cells adjacent to the wound edge. This is in comparison to normal wounds in which proliferation is prominent by 24 hr after wounding, also involving the first 4 rows of cells and by 48 hr, proliferation extends to involve the first 10 rows of cells. In dysfunctional wounds, however, it takes 144 hr after wounding before the first 10 rows of cells begin to actively proliferate. In addition, proliferation occurs deeper in the monolayer and this level is maintained over the next 144 hr, when the wound closes. Thus, when migration is reduced, proliferation becomes prominent and persists to complete repair. However, the overall rate of repair is reduced.
D S Ettenson; A I Gotlieb
Related Documents :
18073097 - Cell models of prion infection.
10984537 - A model for individual and collective cell movement in dictyostelium discoideum.
3455707 - A model for the regulation of myelopoiesis by specific factors.
16125727 - Effects of persister formation on bacterial response to dosing.
9303307 - The anti-apoptosis function of bcl-2 can be genetically separated from its inhibitory e...
4027977 - Depletion of cellular glutathione by exogenous spermine in v79 cells: implications for ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Microvascular research     Volume:  48     ISSN:  0026-2862     ISO Abbreviation:  Microvasc. Res.     Publication Date:  1994 Nov 
Date Detail:
Created Date:  1995-05-30     Completed Date:  1995-05-30     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0165035     Medline TA:  Microvasc Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  328-37     Citation Subset:  IM    
Department of Pathology, Banting and Best Diabetes Centre, University of Toronto, Toronto Hospital Research Institute, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cell Division / drug effects
Cell Movement / drug effects
Cells, Cultured
Cycloheximide / pharmacology
Cytoskeleton / drug effects
Dactinomycin / pharmacology
Endothelium, Vascular / drug effects,  injuries*,  pathology
Reference Values
Transcription, Genetic / drug effects
Wound Healing / drug effects*
Reg. No./Substance:
50-76-0/Dactinomycin; 66-81-9/Cycloheximide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Evaluation of pulsatile and nonpulsatile flow in capillaries of goat skeletal muscle using intravita...
Next Document:  Standard and near-surface laser-Doppler perfusion in foot dorsum skin of diabetic and nondiabetic su...