ArticleLipids in health and disease2011
Targeted metabolomic analyses of cellular models of pelizaeus-merzbacher disease reveal plasmalogen and myo-inositol solute carrier dysfunction.
Article in Lipids in health and disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 19 citations in OpenAlex.
- Impact of dietary myo-inositol supplements on immune cell distribution and cytokine expression in laying hens of two different strains.Poultry science · 2026Article
- Targeted Plasmalogen Supplementation: Effects on Blood Plasmalogens, Oxidative Stress Biomarkers, Cognition, and Mobility in Cognitively Impaired Persons.Frontiers in cell and developmental biology · 2022Article
- Pharmacokinetics, Mass Balance, Excretion, and Tissue Distribution of Plasmalogen Precursor PPI-1011.Frontiers in cell and developmental biology · 2022Article
- Lipids in the Physiopathology of Hereditary Spastic Paraplegias.Frontiers in neuroscience · 2020Review
- Ketogenic diet ameliorates axonal defects and promotes myelination in Pelizaeus-Merzbacher disease.Acta neuropathologica · 2019Article
- EPT1 (selenoprotein I) is critical for the neural development and maintenance of plasmalogen in humans.Journal of lipid research · 2018Article
- From peroxisomal disorders to common neurodegenerative diseases - the role of ether phospholipids in the nervous system.FEBS letters · 2017Review
- Plasmalogen biosynthesis is spatiotemporally regulated by sensing plasmalogens in the inner leaflet of plasma membranes.Scientific reports · 2017Article
- Peroxisomes in brain development and function.Biochimica et biophysica acta · 2016Review
- Mass spectrometry strategies for clinical metabolomics and lipidomics in psychiatry, neurology, and neuro-oncology.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Review
- Topogenesis and homeostasis of fatty acyl-CoA reductase 1.The Journal of biological chemistry · 2013Article
- Region- and age-dependent alterations of glial-neuronal metabolic interactions correlate with CNS pathology in a mouse model of globoid cell leukodystrophy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
- Cellular diamine levels in cancer chemoprevention: modulation by ibuprofen and membrane plasmalogens.Lipids in health and disease · 2011Article
- In vitro and in vivo plasmalogen replacement evaluations in rhizomelic chrondrodysplasia punctata and Pelizaeus-Merzbacher disease using PPI-1011, an ether lipid plasmalogen precursor.Lipids in health and disease · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLeukodystrophies are devastating diseases characterized by dys- and hypo-myelination. While there are a number of histological and imaging studies of these disorders, there are limited biochemical data available. We undertook targeted lipidomic analyses of Pelizaeus-Merzbacher disease (PMD) fibroblasts, PMD lymphocytes, and 158JP oligodendrocytes, a murine model of PMD, to define the lipid changes in these cell models. Further targeted metabolomics analyses were conducted to obtain a preliminary evaluation of the metabolic consequences of lipid changes and gene mutations in these cell models.
resultsIn both PMD fibroblasts and lymphocytes, and 158JP oligodendrocytes, ethanolamine plasmalogens were significantly decreased. Labeling studies with 158JP oligodendrocytes further demonstrated a decreased rate of lipid remodeling at sn-2. Targeted metabolomics analyses of these cells revealed dramatic increases in cellular levels of myo-inositol. Further uptake studies demonstrated increased rates of myo-inositol uptake by PMD lymphocytes.
conclusionsOur data demonstrating PlsEtn decrements, support previous studies indicating leukodystrophy cells possess significant peroxisomal deficits. Our data for the first time also demonstrate that decrements in peroxisomal function coupled with the PLP1 gene defects of PMD, result in changes in the function of membrane myo-inositol solute carriers resulting in dramatic increases in cellular myo-inositol levels.
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