Effect of p53 Deficiency on External Vascular Cuff-Induced Neointima Formation.

Effects of genetic ablation of bach1 upon smooth muscle cell proliferation and atherosclerosis after cuff injury

“…To assess the role of Bach1 in the pathogenesis of atherosclerosis, we evaluated the effects of bach1 ‐deficiency on external vascular cuff‐induced neointima formation (Moroi et al . 1998, 2003).…”

Presence and Severity of Chlamydia pneumoniae and Cytomegalovirus Infection in Coronary Plaques Are Associated With Acute Coronary Syndromes

“…Cytomegalovirus (CMV) infection is also considered to increase the risk of development of CAD, [19][20][21] including a risk of restenosis after balloon angioplasty, 22,23) which may occur through p53 suppression by cytomegalovirus, because the absence of p53 increases vascular neointima formation. 24) Although microorganisms such as Cpn and CMV are thought to be associated with chronic coronary artery disease, the role of these pathogens in the initiation of acute coronary syndromes (ACS) is less well defined.…”

Increased p53 gene dosage reduces neointimal thickening induced by mechanical injury but has no effect on native atherosclerosis

“…Studies in p53-null mice have demonstrated that endogenous p53 expression limits neointimal thickening induced by high-fat feeding [16][17][18][19], vein grafting [20], perivascular cuff placement [21], and mechanical denudation [22]. In line with these findings, transient p53 gene transfer attenuated neointimal lesion formation in balloon-injured rat and rabbit carotid artery [24,25], in porcine interposition vein grafts [26], and in human saphenous vein organ cultures [27].…”

“…First, both global and hematopoietic cell-specific p53 deficiency aggravates atheroma progression in murine models of diet-induced atherosclerosis [16][17][18][19]. Likewise, p53-null mice exhibit accelerated neointimal thickening induced by vein grafting [20], external vascular cuff placement [21], and mechanical denudation [22]. Second, intraluminal antisense p53 oligodeoxynucleotide transfection into intact rat carotid artery promotes vascular SMC growth [23], and p53 gene transfer attenuates neointimal thickening in balloon-injured rat and rabbit carotid artery [24,25], porcine interposition saphenous vein grafts [26], and organ cultures of human saphenous vein [27].…”