Accelerated maximal velocity of the red blood cell Na+/K+ pump in hyperlipidemia is related to increase in 1-palmitoyl, 2-arachidonoyl-plasmalogen phosphatidylethanolamine

Duhm, Jochen; Engelmann, Bernd; Schönthier, Ulrike M.; Streich, Sabine

doi:10.1016/0005-2736(93)90040-7

Cited by 22 publications

(6 citation statements)

References 11 publications

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“…It is well known that the induced changes of cholesterol content in the membrane of human RBC are able to modify kinetic properties (V max , K m for Na i + ) of the Na + -K + pump (Claret et al, 1978). The same is true for the impact of membrane phospholipids on the Na + -K + pump and Na + -K + -2Cl À cotransport in human RBC (Engelmann et al, 1990b;Duhm et al, 1993).…”

Section: Discussionmentioning

confidence: 81%

Relationships between membrane lipids and ion transport in red blood cells of Dahl rats

et al. 2005

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Section: Discussionmentioning

confidence: 81%

Relationships between membrane lipids and ion transport in red blood cells of Dahl rats

et al. 2005

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“…ion channels and ion pumps), and promote membrane fusion through the unique stereoelectronic structure imposed by the vinyl ether linkage at the sn-1 aliphatic chain. [2][3][4][5][6][7] Phospholipases A 2 (PLA 2 s) catalyse the hydrolysis of the sn-2 ester linkage of glycerophospholipids to generate free fatty acid (e.g. AA) and lysolipid products ( Figure 2).…”

Section: Calcium-independent Phospholipase a 2 Bmentioning

confidence: 99%

Eicosanoid signalling pathways in the heart

Jenkins

Cedars

Gross

2008

Cardiovascular Research

161

119

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Myocardial phospholipids serve as primary reservoirs of arachidonic acid (AA), which is liberated through the rate-determining hydrolytic action of cardiac phospholipases A2 (PLA2s). A predominant PLA2 in myocardium is calcium-independent phospholipase A2beta (iPLA2beta), which, through its calmodulin (CaM) and ATP-binding domains, is regulated by alterations in local cellular Ca2+ concentrations and cardiac bioenergetic status, respectively. Importantly, iPLA2beta has been demonstrated to be activated by ischaemia through elevation of the concentration of myocardial fatty acyl-CoA, which abrogates Ca2+/CaM-mediated inhibition of iPLA2beta. AA released by PLA2-catalysed hydrolysis of phospholipids serves as a precursor for eicosanoids generated by pathways dependent on cyclooxygenases (COX), lipoxygenases (LOX), and cytochromes P450 (CYP). Eicosanoids initiate and propagate diverse signalling cascades, primarily through their interaction with cellular receptors and ion channels. However, during pathologic states such as ischaemia or congestive heart failure, eicosanoids contribute to multiple maladaptive changes including inflammation, alterations of cellular growth programmes, and activation of multiple transcriptional events leading to the deleterious sequelae of these pathologic states. This review summarizes the central roles of myocardial PLA(2)s in eicosanoid signalling in the heart, the major COX, LOX, and CYP pathways of eicosanoid generation in the myocardium, and the effects of important eicosanoids on receptor-, ion channel-, and transcription-mediated processes that facilitate cardiac hypertrophy, mediate ischaemic preconditioning, and precipitate arrhythmogenesis in response to pathologic stimuli.

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“…The ethanolamine plasmalogens (PlsEtn) are rich in the brain, testes, and kidney, whereas choline plasmalogens (PlsCho) are rich in cardiac and skeletal muscle [1]. Previous reports suggest that plasmalogens are involved in vesicle formation and membrane fusion [2, 3, 4], ion transport [5,6,7], cholesterol efflux [8], and generation of secondary signal mediators [9,10]. Plasmalogens may also act as an endogenous lipidemic antioxidant, because the vinyl ether substituent at the sn-1 position of the glycerol backbone is highly sensitive to oxidative damage [11,12].…”

Section: Introductionmentioning

confidence: 99%

Composition of plasmalogens in serum lipoproteins from patients with non-alcoholic steatohepatitis and their susceptibility to oxidation

Ikuta

Sakurai

Nishimukai

et al. 2019

Clinica Chimica Acta

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Plasmalogens are ether phospholipids (PL) with an alkenyl group including vinyl ether bound at the sn-1 position and a polyunsaturated fatty acid bound at the sn-2 position, and are susceptible to oxidation. To date, there are no reports on the relationship between plasmalogen in serum lipoproteins and non-alcoholic steatohepatitis (NASH), caused by multiple factors including oxidative stress. Here, we have investigated the distribution of plasmalogens in serum lipoproteins isolated from NASH patients and healthy volunteers. MethodsSerum lipoproteins were separated by gel-filtration chromatography, and analyzed for ethanolamine and choline plasmalogens using liquid chromatography-mass spectrometry. ResultsBoth plasmalogen levels were higher in HDL than in VLDL or LDL. The plasmalogens/PL ratio was significantly lower in NASH than controls, for all lipoprotein fractions. Ethanolamine plasmalogens containing 20:4 and 22:6 at the sn-2 position and choline plasmalogens containing 16:0 at the sn-1 position were 5 predominant in each group. In oxidation test using LDL from healthy serum, both types of plasmalogens were decreased during the early stages of oxidation. ConclusionPlasmalogens could be a potential biomarker for evaluating the early stages of oxidation in NASH.

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Accelerated maximal velocity of the red blood cell Na+/K+ pump in hyperlipidemia is related to increase in 1-palmitoyl, 2-arachidonoyl-plasmalogen phosphatidylethanolamine

Cited by 22 publications

References 11 publications

Relationships between membrane lipids and ion transport in red blood cells of Dahl rats

Relationships between membrane lipids and ion transport in red blood cells of Dahl rats

Eicosanoid signalling pathways in the heart

Composition of plasmalogens in serum lipoproteins from patients with non-alcoholic steatohepatitis and their susceptibility to oxidation

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