Particulate matter increases connexin 43 expression and exacerbates endothelial barrier disruption.

ABSTRACT:

Objectives

Particulate Matter (PM) air pollution is known to exacerbate cardiopulmonary diseases. We previously demonstrated that PM mediates endothelial injury and barrier disruption by modulating the endothelial cytoskeleton and cell-cell junctions, but the effects of PM exposure on cell-cell communication and gap junction activity are still unknown.

Methods

This study focused on the characterization of PM-regulated endothelial dysfunction through connexin 43 (Cx43), the most abundant gap junction protein expressed in lung endothelial cells (ECs), using cultured human lung endothelial cells and a well-characterized PM sample.

Results

PM exposure induced a time-dependent increase of Cx43 in human lung ECs at both the mRNA and protein levels. N-acetylcysteine (NAC), a

SUBMITTER: Zhang J 

PROVIDER: S-EPMC10492082 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature