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HDL has various species, identified on the basis of their major apolipoprotein (apo) components (apoA-I or apoA-II), density (HDL2 and HDL3), and electrophoretic mobility [6].
Julve, "Role of apoA-II in lipid metabolism and atherosclerosis: advances in the study of an enigmatic protein," Journal of Lipid Research, vol.
In vivo interactions of apoA-II, apoA-I, and hepatic lipase contributing to HDL structure and antiatherogenic functions.
Conversely, it enhances the rate of apoA-I and apoA-II synthesis, thereby increasing HDL concentration which is atheroprotective.
Although all HDL subfractions can inhibit caspase-dependent mitochondrial pathway apoptosis to some degree, [HDL.sub.3c] and lipid-free apoA-I have greater antiapoptotic activity than [HDL.sub.2]b or lipid-free apoA-II, respectively (93, 94, 98-100).
Brewer Jr., "Differential tissue-specific expression of human apoA-I and apoA-II," Journal of Lipid Research, vol.
LpA-1:A-II: Lipoproteins containing apoA-I and apoA-II
[16] have studied the apolipoprotein A-II (ApoA-II) that is in forms of 20% of HDL cholesterol and in human it is present about two-thirds of HDL in humans.
The CKD induced hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are primarily due to down regulation of lipoprotein lipase, hepatic lipase, and the very low density lipoprotein receptor, as well as, up regulation of hepatic acyl-CoA cholesterol acyltransferase (ACAT).These abnormalities are compounded by down regulation of apolipoproteins apoA-I, apoA-II and apoC-II in CKD.
Indeed, in such a cohort, apoA-II influenced apoE-linked cardiovascular disease in Dutch women with high levels of HDL-cholesterol and C-reactive protein (13).