LOCAL ADMINISTRATION OF CARBON MONOXIDE INHIBITS NEOINTIMA FORMATION IN BALLOON INJURED RAT CAROTID ARTERIES

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

David A. Tulis (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: Recent studies indicate that systemic induction of heme oxygenase-1 (HO-1) which oxidatively degrades heme into iron biliverdin and carbon monoxide (CO) or adenoviral-mediated gene transfer of HO-1 inhibits neointima formation after experimental vascular injury. In the present study we investigated whether the acute local administration of the HO-1 product CO regulates the arterial remodeling response following injury. Immediately after balloon injury of rat carotid arteries a saturated solution of CO or nitrogen (N2) or phosphate buffered saline (PBS) was incubated luminally within the injured vessels for 30 min. Two weeks after injury rteries exposed to CO exhibited significantly reduced neointimal area neointimal area/medial wall area ratio neointimal thickness and medial wall area compared to arteries exposed to N2 or PBS. Arteries exposed to CO also demonstrated significantly reduced DNA synthesis in the medial wall two days after injury as suggested by proliferating cell nuclear antigen immunostaining and this was associated with a decrease in the protein expression of the G1 cyclins cyclin E and A and transforming growth factor-beta1. These results indicate that the acute local delivery of CO blocks the pathophysiological remodeling response to vascular injury and identifies CO as a potentially important therapeutic agent in the treatment of vasculoproliferative disease.

Additional Information

Publication

Other

Cellular and Molecular Biology (Noisy-le-Grand) 2005 Oct 3;51(5):441-6.

Language: English

Date: 2013

Keywords

Carbon monoxide, balloon injury, neointima, smooth muscle proliferation, cyclins, transforming growth factor-beta1

Email this document to