Disease relevance of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• The function, at the molecular level, of phosphatidylethanolamine, phosphatidylglycerol, and cardiolipin in specific cellular processes is reviewed, with a focus on the results of combined molecular genetic and biochemical studies in Escherichia coli [1].
• Hepatoma nuclei and mitochondria contained only 25% or less the concentrations of phosphatidylethanolamine (PE) as those of liver, whereas ER, PM, and cytosol fractions of hepatoma contained equal or greater concentration of PE than did the corresponding liver fractions [2].
• In vivo externalization of phosphatidylserine and phosphatidylethanolamine in the membrane bilayer and hypercoagulability by the lipid peroxidation of erythrocytes in rats [3].
• Biochemical analysis suggested that heterogeneity in fatty acid composition of phosphatidylethanolamine could influence the degree of Helicobacter binding [4].
• This paper presents a kinetic analysis of low-pH-induced fusion of Semliki Forest virus (SFV) with cholesterol-containing unilamellar lipid vesicles (liposomes), consisting otherwise of phosphatidylcholine, phosphatidylethanolamine and sphingomyelin [5].

Psychiatry related information on DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• Role of head group structure in the phase behavior of amino phospholipids. 2. Lamellar and nonlamellar phases of unsaturated phosphatidylethanolamine analogues [6].
• Duramycin was used to probe the role of PE in mitochondrial energy conversion reactions with the following results: (i) Duramycin uncoupled mitochondrial respiration, decreasing the respiratory control ratio to 1 at 5 microM [7].
• A significant and selective deficiency of ethanolamine plasmalogen (PPE) relative to phosphatidylethanolamine was identified in post mortem brain samples from patients with Alzheimer's disease (AD) [8].
• The age-dependent differences noted in aged Huntington's disease subjects: increased phosphatidylcholine/phosphatidylethanolamine ratio and sphingomyelin + lysophosphatidylcholine content of fibroblast plasma membranes were not significantly altered when compared to normal age-matched controls [9].
• A highly significant (40-70%) reduced rate of esterification of [14C]-AA into PI/PS, PC and PE was found in platelets from patients with schizophreniform, schizoaffective and major depressive disorders but not in platelets from patients with chronic schizophrenia [10].

High impact information on DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• Assays of phospholipid composition reveal that total phosphatidylethanolamine is decreased in eas mutants [11].
• Our results showed that films made of egg lecithin, dioleoyllecithin or phosphatidylethanolamine from two different sources (egg yolk and E. coli) are unadhesive for platelets [12].
• The antitubulins inhibited the incorporation of 3H-methyl groups into phosphatidylethanolamine in guinea pig macrophages and polymorphonuclear leukocytes by as much as 64%, while cytochalasin B, an antimicrofilament agent, had no effect [13].
• Cross-linking of phosphatidylethanolamine films with glutaraldehyde or egg lecithin, as well as dioleoyllecithin with OsO4, abolishes the phase transition of the lipids in these films, transforming them to the solid state [12].
• Apg8 is covalently conjugated to phosphatidylethanolamine through an amide bond between the C-terminal glycine and the amino group of phosphatidylethanolamine [14].

Chemical compound and disease context of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• A plasmid containing the Escherichia coli chloramphenicol acetyltransferase (CAT) gene under the control of a mammalian cAMP-regulated promoter was entrapped in H-2Kk antibody-coated liposomes composed of dioleoyl phosphatidylethanolamine, cholesterol, and oleic acid (pH-sensitive immunoliposomes) [15].
• Influence of chemotherapy administration on monocyte activation by liposomal muramyl tripeptide phosphatidylethanolamine in children with osteosarcoma [16].
• The high-metastatic B16-F10 melanoma cell membranes had lower cholesterol/phospholipid ratios, lower arachidonic acid content, lower polyunsaturated fatty acid content, higher phosphatidylcholine/phosphatidylethanolamine ratios, and higher succinate cytochrome c reductase activity than those of B16-F1 melanoma cell membranes [17].
• These desaturases, when expressed in Escherichia coli, desaturated stearic acid to yield oleic acid at the C-1 positions of phosphatidylethanolamine and phosphatidylglycerol, but did not desaturate palmitic acid, palmitoleic acid, and cis-vaccenic acid [18].
• Several anionic amphiphiles, including cholesterol sulfate, a component of mammalian plasma membranes, lower the final extent of Sendai virus fusion with both human erythrocyte ghosts and liposomes composed of PE and 5% of the ganglioside, GD1a [19].

Biological context of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• For these and other reasons, there is considerable doubt that methylation of phosphatidylethanolamine could account for the many physiological responses attributed to this activity [20].
• Enzymatic methylation of phosphatidylethanolamine increases erythrocyte membrane fluidity [21].
• The appearance of beta-adrenergic binding sites was dependent on the formation of phosphatidylcholine by the enzyme that converts phosphatidyl-N-monomethylethanolamine from phosphatidylethanolamine [22].
• Transmethylation of phosphatidylethanolamine: an initial event in embryonic chicken lens fiber cell differentiation [23].
• Activation of the alternative complement pathway by exposure of phosphatidylethanolamine and phosphatidylserine on erythrocytes from sickle cell disease patients [24].

Anatomical context of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• Furthermore, in conditions where marked changes in microviscosity of the erythrocyte membrane were observed, only extremely small amounts of phosphatidylethanolamine were methylated [20].
• The conversion of phosphatidylethanolamine to phosphatidylcholine was first reported in rat liver microsomes by Bremer and Greenberg [20].
• The external monolayer of the normal red cell membrane contained at least 68 to 72 percent of the total phosphatidylcholine and 15 to 20 percent of the total phosphatidylethanolamine [25].
• Agents that induce differentiation of lens epithelial cells into lens fiber cells in vitro transiently stimulate the transmethylation of phosphatidylethanolamine [23].
• These results identify alterations in phosphatidylethanolamine N-methylation in subcellular membranes from diabetic heart, and it is suggested that these defects may be crucial in the development of cardiac dysfunction in chronic diabetes [26].

Associations of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE with other chemical compounds

• X-ray diffraction and capacitance measurements have been used to calculate the depth to which water penetrates in fully hydrated bacterial phosphatidylethanolamine bilayers in the presence and absence of cholesterol [27].
• The transverse diffusion rate of aminophospholipids is reduced by 41% (phosphatidylserine) and 14% (phosphatidylethanolamine) in homozygote sickle cells (SS) when compared with normal cells (AA) or heterozygote cells (AS or SC) [28].
• The results demonstrate that AcCho can be synthesized from choline derived from the degradation of endogenous PtdCho formed de novo by methylation of phosphatidylethanolamine [29].
• Partially purified plasma membranes prepared from rat adipocytes contain N-methyltransferase(s) that utilize(s) S-adenosyl-L-methionine to synthesize phosphatidylcholine from phosphatidylethanolamine [30].
• Drs2p from budding yeast localizes to the trans-Golgi network (TGN), and here we show that this membrane contains an ATP-dependent APLT that flips 7-nitro-2-1,3-benzoxadiazol-4-yl (NBD) PS and PE derivatives from the luminal to the cytosolic leaflet [31].

Gene context of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• Plasma membrane translocation of fluorescent-labeled phosphatidylethanolamine is controlled by transcription regulators, PDR1 and PDR3 [32].
• These data demonstrated that PDR1 and PDR3 regulate the net rate of M-C6-NBD-PE translocation (flip-flop) and the steady-state distribution of endogenous phosphatidylethanolamine across the plasma membrane [32].
• Compared with phosphatidylcholine and phosphatidylethanolamine, PS was the least active phospholipid binding to human monocyte-derived macrophages and showed no specificity for soluble or membrane-anchored CD14 [33].
• Phosphatidylethanolamine N-methyltransferase (PEMT) is a quatrotopic membrane protein that catalyzes the conversion of phosphatidylethanolamine to phosphatidylcholine through three sequential methylation reactions [34].
• EPT1-derived activity can transfer either phosphocholine or phosphoethanolamine to diacylglcyerol in vitro, but is currently believed to primarily synthesize phosphatidylethanolamine in vivo [35].

Analytical, diagnostic and therapeutic context of DI-STEAROYL-3-SN-PHOSPHATIDYLETHANOLAMINE

• Molecular cloning, germline transformation, and biochemical experiments show that eas mutants are defective in the gene for ethanolamine kinase, which is required for a pathway of phosphatidylethanolamine synthesis [11].
• Because the hydrophobic nature of dilauroyl PE would be inaccessible to periplasmic chemosensors, we suggest that fibrils act as extracellular signal transducers to probe surfaces for insoluble chemical signals [36].
• In ELISA, ACLA showed strong cross-reactivity to both sphingomyelin (SM) and phosphatidylethanolamine (PE), but the inhibition studies showed that ACLA failed to bind the aqueous suspensions of SM, PE, and PE/PC (1:1) [37].
• During reperfusion, phosphatidylethanolamine and its major constituent fatty acids (C 18:0 and C 20:4) are specifically lost from the mitochondrial membrane [38].
• Material with hemagglutinating activity partitioned into the lipid-soluble phase of a Folch partition of the trypsin extract was sensitive to phospholipase C and alkali, and on two-dimensional thin layer chromatography, it co-migrated principally with phosphatidylethanolamine (PE) [39].

References