Particulate matter air pollution disrupts endothelial cell barrier via calpain-mediated tight junction protein degradation.

ABSTRACT:

Background

Exposure to particulate matter (PM) is a significant risk factor for increased cardiopulmonary morbidity and mortality. The mechanism of PM-mediated pathophysiology remains unknown. However, PM is proinflammatory to the endothelium and increases vascular permeability in vitro and in vivo via ROS generation.

Objectives

We explored the role of tight junction proteins as targets for PM-induced loss of lung endothelial cell (EC) barrier integrity and enhanced cardiopulmonary dysfunction.

Methods

Changes in human lung EC monolayer permeability were assessed by Transendothelial Electrical Resistance (TER) in response to PM challenge (collected from Ft. McHenry Tunnel, Baltimore, MD, particle size >0.1 μm). Biochemical assessment of ROS generation and Ca2+ mobiliz

SUBMITTER: Wang T 

PROVIDER: S-EPMC3489700 | biostudies-literature | 2012 Aug

REPOSITORIES: biostudies-literature