Morphological and functional study of human endothelium response to hyperthermia in vitro

Effects of hyperthermia (+42.5 degrees C) on the endothelial monolayer organization, actin cytoskeleton and cell viability have been examined in culture of human aortic endothelial cells (EC). Short-lasting hyperthermia (1-4 hrs) provoked disappearance of stress fibers, redistribution of actin filam...

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Bibliographic Details
Published inAviakosmicheskaia i Äkologicheskaia meditsina Vol. 35; no. 5; p. 40
Main Authors Romanov, Iu A, Kabaeva, N V, Buravkova, L B
Format Journal Article
LanguageRussian
Published Russia (Federation) 2001
Subjects
Aorta - pathology
Aorta - physiopathology
Cells, Cultured
Cyclic AMP - metabolism
Endothelium, Vascular - pathology
Endothelium, Vascular - physiopathology
Fever - physiopathology
Humans
In Vitro Techniques
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Summary:Effects of hyperthermia (+42.5 degrees C) on the endothelial monolayer organization, actin cytoskeleton and cell viability have been examined in culture of human aortic endothelial cells (EC). Short-lasting hyperthermia (1-4 hrs) provoked disappearance of stress fibers, redistribution of actin filaments to the area of cell-to-cell contacts, shape changes and reorganization of the monolayer. It also stimulated formation of intercellular contacts in a preconfluent EC culture. The cAMP content was elevated one hour after heat treatment and then lowered to negligible values (comparing to the basal cAMP level). Long-lasting hyperthermia (6-72 hrs) resulted in EC injury, and damage of endothelial monolayer accompanied by increased Chromium-51 release and almost complete blockade of [3H]-thymidine incorporation into DNA. Addition of cAMP elevating drugs (forskolin, 8-Br-cAMP or isobutylmethylxanthine) into the cell culture medium prevented heat-induced decrease in cAMP concentration, stimulated EC spreading, protected EC from injury, and promoted integrity of endothelial monolayers. Obtained results indicate that long-lasting hyperthermia can be regarded as an additional factor of endothelium injury involved in development of vascular pathology.
ISSN:0233-528X