[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 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.
Romanov
Iu A
IuA
Kabaeva
N V
NV
Buravkova
L B
LB
D001011:Aorta / Q000473:pathology / Q000503:physiopathology; D002478:Cells, Cultured; D000242:Cyclic AMP / Q000378:metabolism; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D005334:Fever / Q000503:physiopathology*; D006801:Humans; D066298:In Vitro Techniques
D000242:Cyclic AMP