Membrane raft-lysosome redox signalling platforms in coronary endothelial dysfunction induced by adipokine visfatin.

ABSTRACT:

Aims

The adipokine visfatin, produced during obesity, has been reported to participate in the development of cardiovascular disease associated with metabolic syndrome. The present study was designed to test a hypothesis that visfatin causes coronary endothelial dysfunction through lysosome trafficking and fusion to cell membranes, membrane raft (MR) clustering, and formation of redox signalosomes.

Methods and results

By using confocal microscopy, it was found that visfatin, but not adiponectin, stimulated NADPH oxidase (NOX) subunits, gp91(phox) aggregation in MR clusters and p47(phox) translocation to these MR clusters in bovine coronary arterial endothelial cells (CAECs), leading to activation of NOX with a 2.5-fold increase in O(2)(·-) production. A signalling lipid, cera

SUBMITTER: Xia M 

PROVIDER: S-EPMC3020127 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature