Influence of plasmalogen deficiency on membrane fluidity of human skin fibroblasts: a fluorescence anisotropy study

Hermetter, Albin; Rainer, Breitling; Ivessa, E.N.; Kalb, Edwin; Loidl, Josef; Roscher, Adelbert A.; Paltauf, F.

doi:10.1016/0005-2736(89)90510-5

Cited by 72 publications

(34 citation statements)

References 21 publications

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“…However previous research mostly focused on red blood cells (Ways and Hanahan, 1964) and platelets, and only recently other cell types like macrophages and granulocytes have moved into focus. Structurally plasmalogens are speculated to play an essential role in regulating membrane dynamics since they can influence membrane fluidity (Glaser and Gross, 1995;Hermetter et al, 1989). Therefore in a recent study the detailed lipid species profile of all major blood cell types was investigated (Leidl et al, 2008).…”

Section: Distribution In Blood Cellsmentioning

confidence: 99%

Plasmalogens the neglected regulatory and scavenging lipid species

Wallner

Schmitz

2011

Chemistry and Physics of Lipids

274

243

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Section: Distribution In Blood Cellsmentioning

confidence: 99%

Plasmalogens the neglected regulatory and scavenging lipid species

Wallner

Schmitz

2011

Chemistry and Physics of Lipids

274

243

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“…Fluidity of plasma membranes was estimated with fluorescence polarization technique (Hermetter et al, 1989). Trimethylammonium-diphenylhexatriene (TMA-DPH) was used as a fluorescence marker.…”

Section: Membrane Fluiditymentioning

confidence: 99%

Inhibition by vitamin E of drug accumulation and of phospholipidosis induced by desipramine and other cationic amphophilic drugs in human cultured cells

Scuntaro

Kientsch

Wiesmann

et al. 1996

British J Pharmacology

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1 Cationic amphiphilic drugs (CADs) are widely used in chronic pharmacotherapies in spite of frequently observed side effects connected with lysosomal phospholipid (PL) storage. 2 It has recently been shown that cx-tocopherol (a-Toc) inhibits drug-and PL accumulation in cell cultures chronically exposed to the CAD, amiodarone. 3 The mechanisms of a-Toc action on drug kinetics and PL storage were studied in human cultured fibroblasts exposed to single and repetitive doses of desipramine and other CADs. 4 a-Toc did not influence the initial, pH-dependent rapid phase of drug uptake. It inhibited, in a dosedependent manner, the slow and the cumulative phases of drug uptake and coincidently the accumulation of cellular PLs. 5 The inhibitory effects of c-Toc on CAD and PL accumulations depends on the ratio between CAD and a-Toc concentrations in the medium. This points to competition between a-Toc and CADs for PL complex formation. 6 Effectiveness of a-Toc on drug uptake varies among different CADs. It depends on its structural integrity but is independent of stereoisomerism. The inhibitory action is restricted to the piggyback slow drug uptake and therefore related to the proportion of membrane-mediated transport to permeation into lysosomes (rapid uptake). This proportion differs among CADs. 7 a-Toc prevents lysosomal membrane-PL storage, accelerates disintegration of PL-stores and normalizes drug-related increased membrane fluidity. This strongly suggests that a-Toc restores membrane recycling, impaired by CAD exposure.8 It remains to be tested in vivo whether cx-Toc reduces CAD side effects without interfering with drug effectiveness.

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“…For AS-30D hepatoma cells, an inverse relationship between SCP-2 concentrations and intracellular cholesterol synthesis has been reported (271, suggesting that SCP-2 is more likely to be involved in cholesterol exchange between plasma membranes than in biosynthesis [28]. Furthermore, the low plasmalogen content of some peroxisomal-disease fibro- blasts [29] is unlikely to be responsible for cholesterol biosynthesis, as in plasmalogen-defective fibroblasts and controls downregulation by LDL occurs to a similar extent (Fig. 4).…”

Section: Discussionmentioning

confidence: 99%

“…4). Supplementation of peroxisomal-disease cells with 1 -0-hexadecyl-sn-glycerol [29], a precursor of plasmalogen biosynthesis, had no effect on intracellular cholesterol concentrations [20]. It is likely that receptor-mediated endocytosis of LDL is not affected by ether-choline glycerophospholipids, a subclass of easily exchangeable and transferable membrane lipids [30-321. The mechanisms underlying the observed increase in cholesterol synthesis by the mutant CHO cell line (Fig.…”

Section: Discussionmentioning

confidence: 99%

Cholesterol biosynthesis in dermal fibroblasts from patients with metabolic disorders of peroxisomal origin

Malle

Oettl

Sattler

et al. 1995

Eur J Clin Investigation

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Abstract. As peroxisomes possess some of the integral enzymes for cholesterol biosynthesis, the role of these organelles in cholesterol formation was studied in dermal fibroblasts with three types of peroxisomal defect: group I, characterized by the absence of intact peroxisomes (neonatal adrenoleukodystrophy, cerebrohepatorenal syndrome of Zellweger); group 11, showing impaired activity of a single peroxisomal enzyme (X-linked adrenoleukodystrophy, adrenomyeloneuropathy); and group 111, defective in more than one peroxisomal enzyme (rhizomelic chondrodysplasia punctata). Cells were incubated with three different radioactive precursors, namely [I4C]-octanoate, [I4C]-acetate, and [3H]-mevalonate, and incorporation of these radiolabels into cholesterol was determined. All fibroblasts with peroxisomal defects were able to form cholesterol at concentrations comparable or higher than those in controls dependent on the radioactive substrate. Binding properties (KD and b, , values) of LDL to fibroblasts with peroxisomal defects and downregulation of intracellular cholesterol biosynthesis were similar to those found in fibroblasts from normolipidaemic controls, but different to those observed in LDL-receptor negative fibroblasts. As our studies revealed that cholesterol biosynthesis is not impaired in fibroblasts from patients with metabolic disorders of peroxisomal origin, we conclude that peroxisomes play little or no role in the pathway of cholesterol synthesis beyond mevalonate. In earlier steps of the cholesterol synthesis pathway, peroxisoma1 and mitochondrial defects in parallel may alter cholesterol synthesis indirectly.

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Influence of plasmalogen deficiency on membrane fluidity of human skin fibroblasts: a fluorescence anisotropy study

Cited by 72 publications

References 21 publications

Plasmalogens the neglected regulatory and scavenging lipid species

Plasmalogens the neglected regulatory and scavenging lipid species

Inhibition by vitamin E of drug accumulation and of phospholipidosis induced by desipramine and other cationic amphophilic drugs in human cultured cells

Cholesterol biosynthesis in dermal fibroblasts from patients with metabolic disorders of peroxisomal origin

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