Disease relevance of Apoa1

• Monomethylethanolamine reduces plasma triacylglycerols and apolipoprotein B and increases apolipoprotein A-I rats without induction of fatty liver [1].
• These results support the concept that HDL is catabolized as a particle mediated by apolipoprotein A-I recognition, and they reinforce earlier work indicating that increased synthesis is the dominant factor responsible for increased plasma HDL concentrations in experimental nephrosis [2].
• In the present study, the cardioprotective effects of synthetic high-density lipoproteins (sHDLs) made of phosphatidylcholine and apolipoprotein A-I were investigated in isolated rat hearts, which underwent a 20-min low-flow ischemia followed by a 30-min reperfusion [3].
• Synthesis of a number of rat liver proteins, including albumin, fibrinogen, apolipoprotein AI, and transferrin, is elevated in the nephrotic syndrome (NS) [4].
• Changes in albumin, fibrinogen, apolipoprotein AI, and transferrin mRNA levels in total cellular RNA isolated from the livers of normal rats and rats with passive Heymann nephritis were measured using a kinetically monitored, reverse transcriptase-initiated PCR (kRT-PCR) assay [4].

High impact information on Apoa1

• A high-affinity HDL receptor for apolipoprotein A-I (apoA-I) was previously identified on the surface of hepatocytes [5].
• Ectopic beta-chain of ATP synthase is an apolipoprotein A-I receptor in hepatic HDL endocytosis [5].
• Role of thyroid hormones in apolipoprotein A-I gene expression in rat liver [6].
• A role for apolipoprotein E, apolipoprotein A-I, and low density lipoprotein receptors in cholesterol transport during regeneration and remyelination of the rat sciatic nerve [7].
• At later times when epithelial cells and lamina propria both contained fat droplets, bright ApoA-I stain surrounded many droplets in the supranuclear cytoplasm of cells and in the lamina propria [8].

Chemical compound and disease context of Apoa1

• Effects of dehydroepiandrosterone on rat apolipoprotein AI gene expression in the human hepatoma cell line, HepG2 [9].
• Induction of the apolipoprotein AI gene by fasting: a relationship with ketosis but not with ketone bodies [10].
• PURPOSE: Although many studies have shown the beneficial effects of lipoproteins on animals with endotoxemia, little is known about the impact of apolipoprotein A-I (apoA-I) on tumor necrosis factor Alpha (TNF-Alpha) release in response to lipopolysaccharide (LPS) [11].

Biological context of Apoa1

• These results indicate that the apolipoprotein A-I/C-III/A-IV multigene family was established before mammalian radiation and suggest that these genes are similarly organized in the genomes of all mammals [12].
• ApoA-I and apoA-IV gene expression was modulated over a 2-fold range, in contrast to the (6-14-fold) pretranslational changes induced by thyroid hormone administration [13].
• We have studied apolipoprotein AI and CIII content of the enterocyte during the course of fat feeding in order to determine their relative synthetic and secretory rates [14].
• Identification of an enhancer-like element in the 5' flanking region of the rat apolipoprotein A-I gene [15].
• One of the proteins was identified as apolipoprotein A-I by N-terminal amino acid sequence analysis [16].

Anatomical context of Apoa1

• Apolipoprotein E mRNA was found in all three cell types, whereas apolipoprotein A-I and A-IV mRNAs were detected only in hepatocytes [17].
• Cholestyramine and a fat-free diet lower apolipoprotein A-IV mRNA in jejunum and cholestyramine lowers apolipoprotein A-I mRNA in ileum of rats [18].
• Abundance of apolipoprotein A-I mRNA in ileal mucosa was comparable to controls in rats fed a fat-free diet but was significantly lower in rats fed cholestyramine [18].
• In the absence of oleic acid, enterocyte secretion of apolipoprotein AI accounted for about half of the apo AI recovered in the medium [14].
• The effects of fat feeding on apolipoprotein AI secretion from rat small intestinal epithelium [14].

Associations of Apoa1 with chemical compounds

• We have characterized the NH2-terminal sequence of the primary translation product of intestinal apolipoprotein A-I mRNA [19].
• In ovariectomized controls, estradiol reduced plasma LDL cholesterol, apolipoprotein B, and fibrinogen and increased apolipoprotein A-I and triglycerides [20].
• The effects of the plasma pattern of GH on serum and lipoprotein levels of total cholesterol, triglycerides, apolipoprotein A-I (apo A-I), apolipoprotein B 48/100 (apo B), and apolipoprotein E (apo E) were studied in hypophysectomized female Sprague-Dawley rats, which had been given replacement therapy with L-T4 and hydrocortisone [21].
• In the presence of oleic acid, the total apolipoprotein AI content of the tissue increased by 50 percent [14].
• Apolipoprotein A-I levels were lowest in the palmitic acid group (oleic and linoleic > palmitic; p < 0.05), and apolipoprotein E levels were highest in the palmitic acid group (palmitic > oleic and linoleic; p < 0.05) [22].

Physical interactions of Apoa1

• However, by competition studies it was found that apolipoprotein A-I competed for the binding to DMPC more effectively than did apolipoprotein A-IV [23].

Other interactions of Apoa1

• Expression of apolipoprotein mRNAs was detected using the polymerase chain reaction and oligonucleotide primers specific for apolipoprotein E, apolipoprotein A-I, and apolipoprotein A-IV [17].
• Regulation of rat liver apolipoprotein A-I, apolipoprotein A-II and acyl-coenzyme A oxidase gene expression by fibrates and dietary fatty acids [24].
• Paraoxonase 1 (PON1) associates to specific high-density lipoproteins (HDLs)--those containing apolipoprotein A-I (apoA-I) and apolipoprotein J (apoJ)--and is largely responsible for their antiatherogenic properties [25].
• Sequence polymorphisms detected between the BN and GK strains in genes encoding ApoAI, AIV, CIII and Lipc do not account for these effects [26].
• Apolipoprotein A-I increases association of cytosolic cholesterol and caveolin-1 with microtubule cytoskeletons in rat astrocytes [27].

Analytical, diagnostic and therapeutic context of Apoa1

• Co-translational cleavage of this in vitro product and NH2-terminal sequence analysis of plasma high density lipoprotein-associated apolipoprotein A-I showed that it is initially synthesized as a preproprotein [19].
• To investigate the effect of bile acids or dietary lipid on the expression of intestinal apolipoproteins, the mRNA levels of apolipoprotein A-I and A-IV in the intestine from rats fed a diet containing cholestyramine or a fat-free diet were compared with those from rats fed a control diet containing 25% casein and 5% corn oil [18].
• Northern blot analysis revealed that the relative concentrations of jejunal apolipoprotein A-I and A-IV mRNA were the same in all groups, whereas ileal apolipoprotein A-I and A-IV mRNA levels were significantly lower in rats fed beet fiber or cholestyramine than in those fed the fiber-free diet [28].
• To determine the effect of free fatty acids on apolipoprotein AI secretion, organ culture explants were incubated for four hours in the presence and absence of 360 microM oleic acid bound to albumin [14].
• Apolipoprotein A-IV was isolated from the d less than 1.21 g/ml fraction of rat serum by gel filtration followed by heparin-Sepharose affinity chromatography; this method also facilitated the preparation of apolipoprotein A-I and apolipoprotein E [23].

References