Inhibition of apoptotic signaling and neointimal hyperplasia by tempol and nitric oxide synthase following vascular injury.

Journal of Vascular Research
Dammanahalli K JagadeeshaRamesh C Bhalla

Abstract

We hypothesized that redox-mediated apoptosis of medial smooth muscle cells (SMC) during the acute phase of vascular injury contributes to the pathophysiology of vascular disease. Apoptosis of medial SMC (1-14 days following balloon injury) was identified in rat carotid arteries by in situ DNA labeling. NADPH-derived superoxide and expression of Bcl-xL, Bax, caspase-3 and caspase-9 were assessed. The antioxidant tempol was administered in drinking water throughout the experimental period, and local adenoviral-mediated gene transfer of eNOS was performed prior to vascular injury. Balloon injury increased NADPH-dependent superoxide production, medial SMC apoptosis, Bax-positive medial SMC index, Bax/Bcl-xL ratio, and caspase-3 and caspase-9 expression in the injured arteries. Treatment with tempol or eNOS gene transfer decreased superoxide levels and medial SMC apoptosis, with a concomitant increase in medial SMC density. Inhibition of superoxide was associated with a decreased Bax/Bcl-xL ratio, and caspase-3 and -9 expression. Tempol treatment and eNOS gene therapy significantly reduced neointima formation. Vascular generation of reactive oxygen species participates in Bax activation and medial SMC apoptosis. These effects likel...Continue Reading

Citations

Sep 10, 2009·Antioxidants & Redox Signaling·Alejandra San Martín, Kathy K Griendling
Jul 14, 2010·Toxicological Sciences : an Official Journal of the Society of Toxicology·Bo JiangTammy R Dugas
May 26, 2009·Expert Opinion on Biological Therapy·Deirdre M O'Connor, Timothy O'Brien
Jan 25, 2017·Expert Opinion on Drug Delivery·Mahmoud A ElnaggarYoon Ki Joung
Jun 16, 2018·American Journal of Physiology. Heart and Circulatory Physiology·Anita MaticInes Drenjancevic

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