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Effect of nicotine and polyaromtic hydrocarbons on cerebral endothelial cells
Author(s) -
Hutamekalin Pilaiwanwadee,
Farkas Attila E.,
Orbók Anna,
Wilhelm Imola,
Nagyőszi Péter,
Veszelka Szilvia,
Deli Mária A.,
Buzás Krisztina,
HunyadiGulyás Éva,
Medzihradszky Katalin F.,
Meksuriyen Duangdeun,
Krizbai István A.
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2007.08.026
Subject(s) - occludin , nicotine , adherens junction , chemistry , phenanthrene , oxidative stress , tight junction , microbiology and biotechnology , biophysics , pharmacology , biochemistry , biology , cadherin , cell , medicine , organic chemistry
The present study was designed to investigate the effect of nicotine and polyaromatic hydrocarbon compounds on cerebral endothelial cells (CECs). Nicotine treatments from 15 min to 5 h 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 −5 M phenanthrene for 24 h 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 24 h treatments with nicotine, methylanthracene or phenanthrene. However, 24 h 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.