Christopher L. Jackson

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RATIONALE High-fat diet with obesity-associated co-morbidities triggers cardiac remodeling and renders the heart more vulnerable to ischemia/reperfusion injury. However, the effect of high-fat diet without obesity and associated co-morbidities is presently unknown. OBJECTIVES To characterize a non-obese mouse model of high-fat diet, assess the(More)
AIMS Vascular smooth muscle cell (VSMC) apoptosis can lead to thinning of the fibrous cap and plaque instability. We previously showed that cell-cell contacts mediated by N-cadherin reduce VSMC apoptosis. This study aimed to determine whether matrix-degrading metalloproteinase (MMP)-dependent N-cadherin cleavage causes VSMC apoptosis. METHODS AND RESULTS(More)
AIMS To examine the roles of the membrane attack complex of complement and its sole membrane regulator, CD59, in atherosclerosis. METHODS C6 (C6(-/-)) deficient and CD59a (Cd59a(-/-)) knockout mice were separately crossed onto the apolipoprotein E knockout (apoE(-/-)) background. The double knockout mice were fed high-fat diet in order to study the(More)
OBJECTIVE Vascular smooth muscle cell (VSMC) proliferation is an important component of atherosclerosis, restenosis after angioplasty and stent placement, and vein graft failure. Outside-in signaling from the cadherin:beta-catenin complex can increase transcription of the cell-cycle gene cyclin D1; however, its role in VSMC proliferation has only recently(More)
Atherosclerosis has been studied in animals for almost a century, yet the events leading up to the rupture of an atherosclerotic plaque (the underlying cause of the majority of fatal thrombosis formation) have only been studied in the past decade, due in part to the development of a mouse model of spontaneous plaque rupture. Apolipoprotein E knockout mice,(More)
Atherosclerosis, the leading cause of death in the Western world, is driven by chronic inflammation within the artery wall. Elements of the complement cascade are implicated in the pathogenesis, because complement proteins and their activation products are found in the atherosclerotic plaque. We examined the role of CD55, a membrane inhibitor of the(More)
BACKGROUND Transglutaminase 2 (TG2), a cross-linking enzyme that confers supra-molecular structures with extra rigidity and resistance against proteolytic degradation, is expressed in the shoulder regions of human atherosclerotic plaques. It has been proposed that TG2 prevents tearing and promotes plaque repair at these potential weak points, and also(More)
AIMS MMPs contribute to atherosclerotic plaque progression and instability, but the relative potency of their endogenous tissue inhibitors of metalloproteinases (TIMPs) as protective factors has not been defined. We therefore investigated the impact of TIMP-1 and TIMP-2 knockout on atherosclerotic plaque burden and composition in apolipoprotein E-knockout(More)
INTRODUCTION The main limitation of coronary artery bypass grafting (CABG) is rapid neointimal hyperplasia leading to graft failure. AIM To assess plaque formation in saphenous vein grafts (SVG) covered by an external Dacron stent in comparison with the classical technique. MATERIAL AND METHODS In the study group vein grafts covered by external stent(More)
OBJECTIVE To investigate the hypothesis that COMP can influence the morphology, stability and size of murine atherosclerotic lesions. METHODS ApoE- and ApoE/COMP-knockout mice were fed a high-fat diet to develop atherosclerotic plaques at lesion sites of three different types; inflammatory and fibrous plaques induced in the carotid artery by low or(More)
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