Previous Article | Next Article ![]()
Clinical and Diagnostic Laboratory Immunology, March 2000, p. 218-225, Vol. 7, No. 2
Department of Microbiology and Immunology and
Division of Bacterial Toxin, Research Center for Infectious Disease,
Aichi Medical University, Nagakute, Aichi 480-1195, Japan
Received 7 September 1999/Accepted 30 December 1999
Morphological changes, especially cytoskeletal alterations, in
lipopolysaccharide (LPS)-induced vascular endothelial cell injury were
studied by using LPS-susceptible bovine aortic endothelial cells
(BAEC). BAEC in cultures with LPS showed cell rounding, shrinking, and
intercellular gap formation. In those cells, LPS caused the
disorganization of actin, tubulin, and vimentin. LPS also induced a
reduction in the F-actin pool and an elevation in the G-actin pool.
Cytoskeletal disorganization affected transendothelial permeability
across the endothelial monolayer. Pretreatment of BAEC with sodium
arsenite (SA) prevented alterations in LPS-induced BAEC injury.
However, posttreatment with SA had no protective effect on them. SA
upregulated the expression of heat shock protein in the presence of
LPS. The role of SA in prevention of LPS-induced BAEC injury is discussed.
1071-412X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Cytoskeletal Alterations in
Lipopolysaccharide-Induced Bovine Vascular Endothelial Cell Injury and
Its Prevention by Sodium Arsenite
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Aichi Medical University, Aichi 480-1195, Japan. Phone: 81 (561) 62-3311. Fax: 81 (561) 63-9187. E-mail: yokochi{at}amugw.aichi-med-u.ac.jp.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»