Abstract
Two main classes of lipoprotein (VLDL and LDL) have functional effects on arterial wall cells. VLDL interacts with endothelial cells and activates the surface-bound enzyme lipoprotein lipase. Lipoprotein-triglyceride is hynrolysed to free fatty acids for transport acroes the endothelium. VLDL is depleted of triglyceride to remnant particles for further catabolism by the liver. Some patients synthesiie an abnormal VLDL with deficiency of apoprotein C-II that fails to activate lipoprotein lipase and they become lipaemic. Other patiente secrete a VLDL with excess apoprotein C-III-2 [40,6 ± 4.2 (6) versus 22.6 ± 2.6 (6) percent total protein for controls], rendering the lipoprotein resistant to hydrolysis by lipoprotein lipaee.VLDL is catabolized to LDL which can penetrate the endothelial barrier. LDL transports cholesterol into arterial wall and other mesenchymal cells. LDL binds with high affinity to specific surface receptors on smooth muscle cells and is taken up and catabolized by the cell. Sterols released from LDL suppress endogenous cholesterol synthesis. Experiments with transcriptional (cardycepin) or translational (cyclohexl-mide) inhibitors suggest that LDL suppresses sterol synthesis at a poet-transcriptional level, i.e. is independent of synthesis of mRNA.
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