Oxidative Stress Induced--Expression Changes of Zonular Occludens--1 in Tight Junction.
10.11637/kjpa.2004.17.4.281
- Author:
Dongsuep SOHN
1
;
Heesang LEE
;
Dajin KIM
;
Hyunhtaek CHOI
;
Kumjeong LEE
;
Hyejin CHO
;
Sukjoong KIM
;
Jongchan LEE
;
Yoonhee JEONG
;
Sungsu KIM
;
Wonbok LEE
;
Kyungyong KIM
Author Information
1. Department of Anatomy, College of Medicine, Chung-Ang University, Korea. skull@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Oxidative stress;
Blood-brain barrier;
Tight junction;
ZO-1
- MeSH:
Blood-Brain Barrier;
Brain;
Cell Death;
Central Nervous System;
Endothelial Cells;
Homeostasis;
Microvessels;
Oxidative Stress*;
Permeability;
Reactive Oxygen Species;
Tight Junctions*
- From:Korean Journal of Physical Anthropology
2004;17(4):281-288
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The homeostasis of microenvironment in central nervous system, essential for normal function, is maintained by blood-brain barrier (BBB). ZO-1 in tight junctions (TJs) plays an important role in maintaining BBB endothelial ion and solute barriers. Malfunction of BBB by reactive oxygen species has been attributed to disruption of TJs. This study examined H2 O2 effects on paracellular permeability and changes in TJ protein ZO-1 using primary culture of bovine brain microvessel endothelial cells. The BBB permeability,measured as TER, increased in a dose-and time-dependent manner when treated with H2O2 (0.01, 0.1, 1.0 mM). Cytotoxicity test revealed that H2O2 did not cause cell death below 1 mM H2 O2 within 4 hr. H2O2 caused intermittent disruption and loss of ZO-1 at tight junctions, but ZO-1 maintained steady state levels of expression. In conclusion, we report that H2O2 induces increased paracellular permeability of BBB that is accompanied with alterations in localization of ZO-1.
