Excessive neointimal formation observed after balloon injury to the rat carotid artery can be prevented by cleaving the mRNA of the early growth response gene, Egr-1, a zinc-finger transcription factor that modulates a host of stress-responsive genes, including PDGF and TGF-, which impact cellular proliferation, migration, and apoptosis. 18 Although the antiproliferative actions of TGF-decrease with age, 19 TGF-suppresses the activity of proteases, activates tissue inhibitors of MMP, and is a potent factor for the synthesis of extracellular matrix proteins. An increase in the expression of TGF-can therefore promote matrix formation. TGF-accumulation in the intima of older rats may be related to the age-associated increase in arterial fibronectin and collagen. 4, 20 Fibronectin and TGF-expression are both regulated by angiotensin II. 21 An age-associated increase in aortic angiotensin converting enzyme (ACE) activity occurs in rats22 and nonhuman primates; aortic angiotensin II is increased and co-localizes with both increased ACE and MMP-2. 23 Importantly, many of the age-associated intimal and matrix changes can be markedly delayed by chronic administration of ACE inhibitors, 3 suggesting that ageassociated changes in the local vascular angiotensin system may play a central role in age-associated vascular remodeling.