Awardee OrganizationSTEWARD ST. ELIZABETH'S MEDICAL CENTER
Description
Abstract Text
DESCRIPTION (Adapted from Investigator's Abstract): Vascular injury has
been shown to induce proliferation and apoptosis in vascular smooth muscle
cells (VSMCs), and this balance between cell growth and cell death will
ultimately influence the size of the injury-induced lesion. Apoptotic cell
death has been documented in human atherectomy and endarterectomy specimens
and in a number of animal models of vessel wall stenosis. Recently, they
have shown that as early as 30 minutes following balloon injury VSMCs of rat
carotid and rabbit iliac arteries undergo apoptotic cell death at a high
frequency as demonstrated by TUNEL staining, and by the appearance of
condensed chromatin and other morphological features characteristic of
apoptosis in electron micrographs. This induction of apoptosis coincides
with a marked downregulation of the bcl-X protein, a potential cell death
antagonist. Their data suggest that VSMC apoptosis is a rapid and prominent
cellular response to acute vascular wall injury, the extent of this
apoptotic response may ultimately influence characteristics of the lesion
that result from the insult. To more fully understand the regulation and
the role of apoptosis in vessel wall lesion formation, it is proposed to:
1) determine the frequencies of VSMC apoptosis in single injury and
double-injury model of angioplasty in rabbit external iliac arteries; 2)
assess the effects of enhanced apoptosis on vessel lesion formation using a
replication defective adenovirus encoding Fas ligand; 3) characterize
apoptosis in a mouse model of arterial injury; and 4) study the mechanisms
that coordinate cell cycle and apoptosis at a molecular level.
No Sub Projects information available for 5R01AG015052-02
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