Korean J Phys Anthropol.  2004 Dec;17(4):281-288.

Oxidative Stress Induced--Expression Changes of Zonular Occludens--1 in Tight Junction

Affiliations
  • 1Department of Anatomy, College of Medicine, Chung-Ang University, Korea. skull@cau.ac.kr
  • 2Department of Thoracic & Cardiovascular Surgery, College of Medicine, Chung-Ang University, Korea.

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.

Keyword

Oxidative stress; Blood-brain barrier; Tight junction; ZO-1

MeSH Terms

Blood-Brain Barrier
Brain
Cell Death
Central Nervous System
Endothelial Cells
Homeostasis
Microvessels
Oxidative Stress*
Permeability
Reactive Oxygen Species
Tight Junctions*
Reactive Oxygen Species
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