Premium
HIV‐1 protein expression increases superoxide and alters aortic endothelial cell function
Author(s) -
Kline Erik Robert,
Walp Erik R.,
Dikalov Sergey,
Kleinhenz Dean J.,
Hart C. Michael,
Sutliff Roy L.
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a816-c
Vascular disturbances are reported in HIV patients. Data suggest that HIV proteins induce a state of oxidative stress. Reactive oxygen species (ROS) production is associated with nitric oxide (NO) depletion and is a catalyst for cardiovascular complications. The present study addresses the impact of HIV‐1 protein expression on endothelial signaling/function, and determines the role ROS play in this effect using an HIV‐1 transgenic rat model (TG). Compared to wild‐type aortas, TG aortas have decreased sensitivity to the endothelium‐dependent vasorelaxant acetylcholine, but not to the NO‐donor sodium nitroprusside. TG aortas produce more superoxide as determined by dihydroethidium staining and electron spin resonance (ESR). Fe(DETC) 2 measurements of NO indicate that NO production is decreased in TG aortas. Systemic markers of endothelial NO including serum nitrite and NO‐hemoglobin are also reduced in TG rats. TG aortas also show diminished phosphorylation of endothelial NO synthase (eNOS) at Ser‐1177 suggesting that eNOS activity may be affected by HIV‐1 proteins. These data suggest that HIV protein expression results in increased ROS and decreased NO which may promote endothelial cell dysfunction.