Effect of nicotine and polyaromtic hydrocarbons on cerebral endothelial cells.
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 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 x 10(-5)M 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.
Hutamekalin
Pilaiwanwadee
P
Institute of Biophysics, Biological Research Centre, Temesvári krt. 62, 6726 Szeged, Hungary.
Farkas
Attila E
AE
Orbók
Anna
A
Wilhelm
Imola
I
Nagyoszi
Péter
P
Veszelka
Szilvia
S
Deli
Mária A
MA
Buzás
Krisztina
K
Hunyadi-Gulyás
Eva
E
Medzihradszky
Katalin F
KF
Meksuriyen
Duangdeun
D
Krizbai
István A
IA
D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology; D015820:Cadherins / Q000378:metabolism; D002540:Cerebral Cortex / Q000166:cytology*; D062507:Claudin-5; D018920:Coculture Techniques; D042783:Endothelial Cells / Q000187:drug effects*; D008565:Membrane Proteins / Q000378:metabolism; D008969:Molecular Sequence Data; D009285:Naphthoquinones / Q000494:pharmacology; D009457:Neuroglia / Q000166:cytology; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D062793:Occludin; D018384:Oxidative Stress; D010616:Phenanthrenes / Q000494:pharmacology; D010750:Phosphoproteins / Q000378:metabolism; D011084:Polycyclic Aromatic Hydrocarbons / Q000494:pharmacology*; D020543:Proteome / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D062826:Zonula Occludens-1 Protein; D062827:Zonula Occludens-2 Protein; D051176:beta Catenin / Q000378:metabolism
D015820:Cadherins; D062507:Claudin-5; C491510:Cldn5 protein, rat; D008565:Membrane Proteins; D009285:Naphthoquinones; D018722:Nicotinic Agonists; D062793:Occludin; C568987:Ocln protein, rat; D010616:Phenanthrenes; D010750:Phosphoproteins; D011084:Polycyclic Aromatic Hydrocarbons; D020543:Proteome; C569044:Tjp1 protein, rat; D062826:Zonula Occludens-1 Protein; D062827:Zonula Occludens-2 Protein; D051176:beta Catenin; C031181:phenanthrene; C063002:2,3-dimethoxy-1,4-naphthoquinone; D009538:Nicotine