The Renin-Angiotensin System Is Involved in the Production of Plasminogen Activator Inhibitor Type 1 by Cultured Endothelial Cells in Response to Chylomicron Remnants

Patients with CD36 Deficiency Are Associated with Enhanced Atherosclerotic Cardiovascular Diseases

“…Furthermore, as nicely reviewed by Fujioka et al 29) , increased remnant lipoproteins (mainly chylomicron remnants) contribute to form atherosclerotic lesions through a variety of mechanisms. It was demonstrated that chylomicron remnants invade directly into the subendothelial spaces of arteries and are taken up by macrophages via several receptors, such as LDL receptor-related protein (LRP) or apoB-48 receptor, resulting in macrophage foam cell formation [30][31][32][33] . We reported that increased serum chylomicron remnants are directly associated with enhanced carotid atherosclerosis in subjects with apparently normal TG levels 34) .…”

“…We reported that increased serum chylomicron remnants are directly associated with enhanced carotid atherosclerosis in subjects with apparently normal TG levels 34) . Chylomicron remnants induce the secretion of monocyte chemoattractant protein 1 (MCP-1), which stimulates the migration of monocytes through arterial endothelial layers 35) and the production of plasminogen activator inhibitor-(PAI-), which regulates thrombus formation on endothelial cells 33) . Thus, abundant chylomicron remnants in the blood of CD36-D patients might enhance the foam cell formation of CD36-deficient macrophages, leading to the development of atherosclerotic cardiovascular diseases.…”

Chylomicron Remnants Stimulate Release of Interleukin-1.BETA. by THP-1 Cells

“…Chylomicrons and chylomicron remnants were separated from rat mesenteric lymph as previously described (5)(6)(7)(8)24). Briefly, chylomicrons were isolated by ultracentrifugation from lymph collected from gastrostomized male Sprague-Dawley rats fed an egg suspension for 48 h. These functionally hepatectomized rats then were injected intravenously with the chylomicrons, and finally exsanguinated after 3 h. Chylomicron remnants were isolated from the plasma by ultracentrifugation.…”

“…The biologic mechanisms by which lipids induce the vascular inflammation, cellular proliferation, lipid deposition, and fibrosis that characterize atherosclerosis remain largely unknown, but recent findings suggest that oxidative modification of low-density lipoproteins (LDL) is a key contributor to the progression of atherosclerosis (1,2). On the other hand, triglyceride-rich lipoprotein particles including chylomicron remnants are also atherogenic (3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Chylomicron remnants are derived from chylomicrons through lipoprotein lipase-mediated hydrolysis of triglycerides in these particles.…”

Comparative Effects of Candesartan and Amlodipine in a Monkey Atherosclerotic Model

“…Chobanian et al (3) reported that a high dose of an ACE inhibitor, trandolapril, reduced the atherosclerotic area in Watanabe heritable hyperlipidemic rabbits with a reduction in blood pressure, but that a low dose of the drug neither decreased atherosclerosis nor blood pressure. molecules and plasminogen activator inhibitor type 1, and the reduction of endothelial function via suppression of nitric oxide synthesis (9)(10)(11)(12)(13)(14). However, it has been unclear whether hypotensive effects improve atherosclerosis in primates.…”