Activation of NAD(P)H oxidase by tryptophan-derived 3-hydroxykynurenine accelerates endothelial apoptosis and dysfunction in vivo.

ABSTRACT:

Rationale

The kynurenine (Kyn) pathway is the major route for tryptophan (Trp) metabolism in mammals. The Trp-Kyn pathway is reported to regulate several fundamental biological processes, including cell death.

Objective

The aim of this study was to elucidate the contributions and molecular mechanism of Trp-Kyn pathway to endothelial cell death.

Methods and results

Endogenous reactive oxygen species, endothelial cell apoptosis, and endothelium-dependent and endothelium-independent vasorelaxation were measured in aortas of wild-type mice or mice deficient for nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase subunits (p47(phox) or gp91(phox)) or indoleamine-pyrrole 2,3-dioxygenase 1 with or without angiotensin (Ang) II infusion. As expected, AngII increased

SUBMITTER: Wang Q 

PROVIDER: S-EPMC4104160 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature