In 1951, McArdle described a glycogen storage disorder which presents primarily as a myopathy. It is characterized by muscle pain, weakness and exercise intolerance with elevated creatine kinase from rhabdomyolysis. The pathophysiology involves a deficiency of myophosphorylase enzyme resulting in an inability to degrade glycogen stores. We present a novel case of McArdle disease (glycogen stora...

We have expressed the extracellular regions of the low-density-lipoprotein (LDL) receptor and the very-low-density-lipoprotein (VLDL) receptor, along with the full-length forms of the receptors, in insect cells in a baculovirus system. The extracellular region of the LDL receptor has been secreted successfully into the culture medium, and it retained the capacities of binding 125I-labelled LDL ...

Rat serum very low density lipoprotein (VLDL) inhibits initiation of DNA synthesis in fetal rat hepatocyte cultures; cells engaged in synthesizing DNA resist inhibition. VLDL action is specific and apparently blocks prereplicative protein synthesis. These and other results, from studies of altered blood VLDL levels and [3H] thymidine incorporation into isolated liver nuclei in 70% hepatectomize...

Cultured rabbit aortic and human carotid artery endothelial cells produced a factor that was chemotactic for monocytes but not for neutrophils. Checkerboard analysis showed that the activity was due to chemotaxis and not to chemokinesis. The factor was produced in both serum-containing and serumless media. Treatment with carboxypeptidase and trypsin resulted in inhibition of chemotactic activit...

In this study, we tested the hypothesis that two separate pathways, the two-step process and an apolipoprotein B (apoB) size-dependent lipidation process, give rise to different lipoproteins. Expression of apoB-100 and C-terminally truncated forms of apoB-100 in McA-RH7777 cells demonstrated that VLDL particles can be assembled by apoB size-dependent linear lipidation, resulting in particles wh...

Little is known regarding the molecular mechanisms of atherogenicity of triglyceride-rich lipoproteins such as very low-density lipoproteins (VLDLs). We examined the effect of VLDL on proliferation of rat aortic smooth muscle cells, intracellular Ca2+ handling, and activity of cAMP-responsive element binding protein (CREB) and nuclear factor of activated T cells (NFAT) transcription factors. VL...

beta-very low density lipoprotein (VLDL) is a large lipoprotein with multiple apoprotein E (apoE) molecules that bind to the LDL receptors on mouse macrophages. Even though they bind to the same receptor, the endocytic processing of beta-VLDL differs from low density lipoprotein (LDL). LDL is rapidly delivered to perinuclear lysosomes and degraded, but much of the beta-VLDL is retained in perip...

High plasma levels of VLDL are associated with increased risk for atherosclerosis. Here we show that VLDL (75 to 150 mg/mL) activates nuclear factor-kB (NF-kB), a transcription factor known to play a key role in regulation of inflammation. Oxidation of VLDL reduced its capacity to activate NF-kB in vitro, whereas free fatty acids such as linoleic and oleic acid activated NF-kB to the same exten...

Hepatocytes were obtained by collagenase perfusion of adult rat liver in situ and plated as monolayers in plastic culture dishes. [3H]Glycerol was actively incorporated into cellular triglycerides and phospholipids which were rapidly secreted into the culture medium. More than 95% of the 3H-triglyceride secreted into the medium was recovered in the very low density lipoprotein (VLDL) fraction (...

Addition of apolipoprotein (apo) E to rabbit beta-very low density lipoproteins (beta-VLDL) has been shown to result in a marked enhancement of their binding and uptake by various cell types. Apolipoprotein E binds to lipoprotein receptors and proteoglycans. To distinguish between apoE binding to these sites, cells were treated with heparinase. Heparinase treatment of receptor-negative familial...