This article is available online at http://www.jlr.org teins (VLDL) from liver. From a clinical perspective, plasma apoB100 levels and the apoB100/apoA1 ratio are superior to any other lipoprotein-related indices used to estimate risk of acute myocardial infarction ( 1 ). This illustrates the need for a deep understanding of the cellular mechanisms that regulate apoB100 production and secretion. Although rat hepatoma McA-RH7777 cells secrete much of their apoB100 as buoyant VLDL, it would be desirable to have a similar cell line of human origin. Many studies of human apoB100 metabolism have used the hepatoma HepG2 cell line. Despite their general use, however, HepG2 cells secrete relatively dense, lipid-poor apoB100-containing particles, unlike the buoyant VLDL particles secreted in vivo by mammalian liver. An alternative human cell model with a more native level of VLDL secretion would strongly benefi t the lipoprotein fi eld and might advance novel insights into apoB100 metabolism.Recently, Huh-7 cells were proposed as a superior human hepatic cell model for the study of apoB100 metabolism and VLDL secretion [see references 2, 3)] and are becoming more widely used for these purposes [see references ( 4, 5 )]. To our knowledge, however, there have been no published studies of the basic characteristics of Huh-7 cells with regard to apoB100 and VLDL metabolism. In the present report, we have fi lled this gap in knowledge and also have compared the results to those with HepG2 cells. Based on the available evidence, Huh-7 cells resemble HepG2 cells in many respects, with neither cell Apolipoprotein-B100 (apoB100) is the essential protein for the assembly and secretion of very low density lipopro- Abbreviations: apoB100, apolipoprotein-B100; MEK-ERK, mitogenactivated protein kinase kinase-extracellular signal regulated kinase; MTP, microsomal triglyceride transfer protein; OA, oleic acid.
Calcific aortic valve stenosis (CAVS) is common in the ageing population and set to become an increasing economic and health burden. Once present, it inevitably progresses and has a poor prognosis in symptomatic patients. No medical therapies are proven to be effective in holding or reducing disease progression. Therefore, aortic valve replacement remains the only available treatment option. Improved knowledge of the mechanisms underlying disease progression has provided us with insights that CAVS is not a passive disease. Rather, CAVS is regulated by numerous mechanisms with a key role for calcification. Aortic valve calcification (AVC) is actively regulated involving cellular and humoral factors that may offer targets for diagnosis and intervention. The discovery that the vitamin K-dependent proteins are involved in the inhibition of AVC has boosted our mechanistic understanding of this process and has opened up novel avenues in disease exploration. This review discusses processes involved in CAVS progression, with an emphasis on recent insights into calcification, methods for imaging calcification activity, and potential therapeutic options.
A diurnal cTnT rhythm substantiates the recommendation that all dynamic changes in cTnT should be interpreted in relation to the clinical presentation. Epidemiological studies and risk-stratification protocols with the use of cTnT may benefit from standardized sampling times. (Exercise and Glycemic Control in Type 2 Diabetes; NCT00945165).
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