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Cancer Cell death Cell cycle Cytoskeleton Exo/endocytosis Differentiation Division Organelles Signalling Stem cells Trafficking
Cell Biology International (2008) 32, 198–209 (Printed in Great Britain)
Effect of nicotine and polyaromtic hydrocarbons on cerebral endothelial cells
Pilaiwanwadee Hutamekalinab, Attila E. Farkasa, Anna Orbóka, Imola Wilhelma, Péter Nagyőszia, Szilvia Veszelkaa, Mária A. Delia, Krisztina Buzásc, Éva Hunyadi‑Gulyásc, Katalin F. Medzihradszkycd, Duangdeun Meksuriyenb and István A. Krizbaia*
aInstitute of Biophysics, Biological Research Centre, Temesvári krt. 62, 6726 Szeged, Hungary
bDepartment of Biochemistry, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Phayathai Road, Pathumwan, Bangkok 10330, Thailand
cProteomics Research Group, Biological Research Centre, Temesvári krt. 62, 6726 Szeged, Hungary
dDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94143-0446, USA


Abstract

The present study was designed to investigate the effect of nicotine and polyaromatic hydrocarbon compounds on cerebral endothelial cells (CECs). Nicotine treatments from 15min to 5h did not cause any changes in the expression and localization of principal junctional proteins. One day of treatment with a relatively high concentration of nicotine induced a decrease in the expression of the tight junction protein ZO-1, occludin, and the adherens junction protein, cadherin. Treatment with 3×10−5M phenanthrene for 24h caused a redistribution of occludin from the Triton X-100 insoluble to the Triton X-100 soluble fraction. Transendothelial electrical resistance was not significantly affected by 24h treatments with nicotine, methylanthracene or phenanthrene. However, 24h nicotine treatment increased transendothelial permeability in CECs exposed to oxidative stress. Both nicotine and phenanthrene were able to regulate the expression of a large number of proteins as revealed by 2D electrophoresis. Our experiments suggest that tobacco smoking may affect the junctional complex of CECs, and that this effect is enhanced by oxidative stress.


Key words: Nicotine, Blood–brain barrier, Cerebral endothelial cells, Polyaromatic hydrocarbons, Tight junction, Proteomics.

*Corresponding author. Tel.: +36 62 599 602; fax: +36 62 433 133.


Received 12 April 2007/18 July 2007; accepted 29 August 2007

doi:10.1016/j.cellbi.2007.08.026


ISSN Print: 1065-6995
ISSN Electronic: 1095-8355
Published by Portland Press Limited on behalf of the International Federation for Cell Biology (IFCB)