Homeostasis of phospholipids

• Verfasst von: Dorninger, Fabian [VerfasserIn]
• Verfasst von: Brodde, Alexander [VerfasserIn]
• Verfasst von: Braverman, Nancy E. [VerfasserIn]
• Verfasst von: Moser, Ann B. [VerfasserIn]
• Verfasst von: Just, Wilhelm W. [VerfasserIn]
• Verfasst von: Forss-Petter, Sonja [VerfasserIn]
• Verfasst von: Brügger, Britta [VerfasserIn]
• Verfasst von: Berger, Johannes [VerfasserIn]
• Titel: Homeostasis of phospholipids
• Titelzusatz: the level of phosphatidylethanolamine tightly adapts to changes in ethanolamine plasmalogens
• Verf.angabe: Fabian Dorninger, Alexander Brodde, Nancy E. Braverman, Ann B. Moser, Wilhelm W. Just, Sonja Forss-Petter, Britta Brügger, Johannes Berger
• Jahr: 2015
• Jahr des Originals: 2014
• Umfang: 12 S.
• Fussnoten: Available online: 15 November 2014 ; Gesehen am 22.06.2020
• Titel Quelle: Enthalten in: Biochimica et biophysica acta / Molecular and cell biology of lipids
• Ort Quelle: Amsterdam : Elsevier, 1998
• Jahr Quelle: 2015
• Band/Heft Quelle: 1851(2015), 2, Seite 117-128
• ISSN Quelle: 1879-2618
• DOI: doi:10.1016/j.bbalip.2014.11.005
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Alzheimer's disease
• Sach-SW: Arachidonic acid
• Sach-SW: Compensation
• Sach-SW: Docosahexaenoic acid
• Sach-SW: Peroxisome
• Sach-SW: Plasmalogen
• K10plus-PPN: 1701698455

Abstract

Ethanolamine plasmalogens constitute a group of ether glycerophospholipids that, due to their unique biophysical and biochemical properties, are essential components of mammalian cellular membranes. Their importance is emphasized by the consequences of defects in plasmalogen biosynthesis, which in humans cause the fatal disease rhizomelic chondrodysplasia punctata (RCDP). In the present lipidomic study, we used fibroblasts derived from RCDP patients, as well as brain tissue from plasmalogen-deficient mice, to examine the compensatory mechanisms of lipid homeostasis in response to plasmalogen deficiency. Our results show that phosphatidylethanolamine (PE), a diacyl glycerophospholipid, which like ethanolamine plasmalogens carries the head group ethanolamine, is the main player in the adaptation to plasmalogen insufficiency. PE levels were tightly adjusted to the amount of ethanolamine plasmalogens so that their combined levels were kept constant. Similarly, the total amount of polyunsaturated fatty acids (PUFAs) in ethanolamine phospholipids was maintained upon plasmalogen deficiency. However, we found an increased incorporation of arachidonic acid at the expense of docosahexaenoic acid in the PE fraction of plasmalogen-deficient tissues. These data show that under conditions of reduced plasmalogen levels, the amount of total ethanolamine phospholipids is precisely maintained by a rise in PE. At the same time, a shift in the ratio between ω-6 and ω-3 PUFAs occurs, which might have unfavorable, long-term biological consequences. Therefore, our findings are not only of interest for RCDP but may have more widespread implications also for other disease conditions, as for example Alzheimer's disease, that have been associated with a decline in plasmalogens.