title: Expression and induction of the stress protein alpha-B-crystallin in vascular endothelial cells.
abstract: Stress-induced development of enhanced tolerance against various kinds of stresses has been observed in vascular endothelial cells as well as in several other cell types. Stress proteins are thought to play a key role in the development of stress tolerance. In this study we show that endothelial cells of various sources contain the major stress protein of the eye lens, alphaB-crystallin. In the mouse myocardial microvascular cell line, MyEnd, alphaB-crystallin as well as the heat shock proteins HSP 70i and HSP 25 display a low constitutive expression but can be significantly upregulated by sodium arsenite stress. Osmotic stress also resulted in strong upregulation of alphaB-crystallin and HSP 70i but not of HSP 25. Both osmotic and arsenite stress resulted in significant stress tolerance of MyEnd cells against glucose deprivation as assayed by lactate dehydrogenase release and overall cellular morphology. Development of stress tolerance without induction of HSP 25 indicates that HSP 25 is not essential for the protective effect. MyEnd cells from alphaB-crystallin-/- mice displayed a similar degree of stress tolerance showing that alphaB-crystallin is dispensable for protection of cells against energy depletion. The functional role of alphaB-crystallin in endothelial cells needs to be further elucidated. In our experiments HSP 70i turned out to be the only potential candidate of the stress proteins assayed to be involved in the development of tolerance against energy depletion.
authors.affiliation: Institute of Anatomy and Cell Biology, Julius-Maximilians-University, Koellikerstrasse 6, 97070 Würzburg, Germany. nikola.golenhofen@mail.uni-wuerzburg.de
authors.forename: Nikola
authors.initials: N
authors.lastname: Golenhofen
authors.forename: Winfried
authors.initials: W
authors.lastname: Ness
authors.forename: Eric F
authors.initials: EF
authors.lastname: Wawrousek
authors.forename: Detlev
authors.initials: D
authors.lastname: Drenckhahn
mesh_terms: D000818:Animals; D015703:Antigens, CD; D018053:Arsenites / Q000494:pharmacology; D015153:Blotting, Western; D015820:Cadherins / Q000096:biosynthesis; D002460:Cell Line; D002478:Cells, Cultured; D003459:Crystallins / Q000096:biosynthesis*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006358:Hot Temperature; D006801:Humans; D009637:Masoprocol / Q000494:pharmacology; D051379:Mice; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis; D012965:Sodium Chloride / Q000494:pharmacology; D017670:Sodium Compounds / Q000494:pharmacology; D013552:Swine; D000099152:Cadherin 5
chemical_list: D015703:Antigens, CD; D018053:Arsenites; D015820:Cadherins; D003459:Crystallins; D006360:Heat-Shock Proteins; D009637:Masoprocol; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012965:Sodium Chloride; D017670:Sodium Compounds; D000099152:Cadherin 5; C017947:sodium arsenite