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175 results for “Lipidomics”

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zenodo36/100

Lipidomics of exosomes derived from granulosa cells

The mapped data files generated from the analysis of the pathway in MetExploreViz. Lipid content categorized by saturation level.

opencc-by-4.0Jun 2024View details →

zenodo36/100

Lipidomic analysis DELISA study fasting and refeeding

This dataset contains complete data from untargeted lipidomic analysis of subcutaneous adipose tissue from premenopausal women. The clinical study providing the samples is described in https://doi.org/10.1016/j.heliyon.2024.e37875

opencc-by-4.0Sep 2024View details →

zenodo36/100

Substantial contribution of in-situ produced bacterial sphingolipids to the sedimentary lipidome

Abstract: The sedimentary lipid pool comprises a myriad of components with some specific biomarkers used in paleoclimatic and geobiological reconstructions. However, a comprehensive view of the sedimentary lipidome is lacking. Here we conduct an untargeted analysis of the Black Sea sedimentary lipidome using high resolution mass spectrometry. Besides commonly reported phytoplankton-derived fossil lipids originate from oxic surface water, a diverse and abundant set of sphingolipids, accounting for ~20% of the lipidome, was discovered. These sphingolipids are produced in-situ by sedimentary anaerobic bacteria, likely in place of phospholipids due to the deficiency of phosphate in anoxic sediments. Our results suggest that while phytoplankton-derived lipids contribute 50–60% of the sedimentary lipidome, the importance of bacterial lipids, particularly in-situ produced sphingolipids, has been overlooked. Source data: Data 1. Spt_hits.and.backbone_sequences.MAFFT-L-INS-i.msa Data 2. Spt_hits.and.backbone_sequences.MAFFT-L-INS-i.msa.trimAl

opencc-by-4.0Nov 2024View details →

dryad36/100

Lipidomic datasets for: Transmembrane protein 135 regulates lipid homeostasis through its role in peroxisomal DHA metabolism

Transmembrane protein 135 (TMEM135) is thought to participate in the cellular response to increased intracellular lipids yet no defined molecular function for TMEM135 in lipid metabolism has been identified. In this study, we performed a lipid analysis of tissues from Tmem135 mutant mice and found striking reductions of docosahexaenoic acid (DHA) across all Tmem135 mutant tissues, indicating a role of TMEM135 in the production of DHA. Since all enzymes required for DHA synthesis remain intact in Tmem135 mutant mice, we hypothesized that TMEM135 is involved in the export of DHA from peroxisomes. The Tmem135 mutation likely leads to the retention of DHA in peroxisomes, causing DHA to be degraded within peroxisomes by their beta-oxidation machinery. This may lead to generation or alteration of ligands required for the activation of peroxisome proliferator-activated receptor a (PPARa) signaling, which in turn could result in increased peroxisomal number and beta-oxidation enzymes observed in Tmem135 mutant mice. We confirmed this effect of PPARa signaling by detecting decreased peroxisomes and their proteins upon genetic ablation of Ppara in Tmem135 mutant mice. Using Tmem135 mutant mice, we also validated the protective effect of increased peroxisomes and peroxisomal beta-oxidation on the metabolic disease phenotypes of leptin mutant mice which has been observed in previous studies. Thus, we conclude that TMEM135 has a role in lipid homeostasis through its function in peroxisomes.

opencc-zeroDec 2022View details →

dryad36/100

Data from: Lipidome modulation by dietary omega-3 polyunsaturated fatty acid supplementation or selective soluble epoxide hydrolase inhibition suppresses rough LPS-accelerated glomerulonephritis in lupus-prone mice

Lipopolysaccharide (LPS)-accelerated autoimmune glomerulonephritis (GN) in lupus-prone NZBWF1 mice is a preclinical model that is potentially applicable for investigating lipidome-modulating interventions. LPS can be expressed as one of two chemotypes: smooth LPS (S-LPS) and rough LPS (R-LPS) which is devoid of O-antigen polysaccharide sidechain. Since these chemotypes differentially affect TLR4-mediated immune cell responses, these differences may influence GN induction. Therefore, we initially compared the effects of subchronic i.p. injection for 5 wk with 1) Salmonella S-LPS, 2) Salmonella R-LPS, or 3) saline vehicle (VEH) (Study 1) in female NZBWF1 mice. R-LPS induced robust elevations in blood urea nitrogen, proteinuria, and hematuria that were not evident in VEH- or S-LPS-treated mice. Histopathologic examination of R-LPS-treated mice one week after final injection further revealed more robust hypertrophy, hyperplasia, thickened membranes, lymphocytic accumulation containing B and T cells, and glomerular IgG deposition consistent with GN but not in VEH- or S-LPS-treated groups. R-LPS but not S-LPS induced spleen enlargement with lymphoid hyperplasia as well as modest inflammatory cell recruitment in the liver. We next employed our optimized R-LPS model to discern the impact of two lipidome-modulating interventions, omega-3 polyunsaturated fatty acid (PUFA) supplementation and soluble epoxide hydrolase (sEH) inhibition, on GN (Study 2). Specifically, the effects of consuming the omega-3 PUFA docosahexaenoic acid (DHA) (10 g/kg diet) and/or the sEH inhibitor TPPU (22.5 mg/kg diet) on R-LPS triggering were compared. Resultant blood fatty acid profiles and epoxy fatty acid concentrations reflected the anticipated DHA- and TPPU-mediated lipidome changes. The relative rank order of R-LPS-induced GN severity among groups fed experimental diets based on proteinuria, hematuria, histopathologic scoring, and glomerular IgG deposition was: VEH/CON < R-LPS/DHA ≈ R-LPS/TPPU <<< R-LPS/ TPPU+DHA ≈ R-LPS/CON. These interventions had modest to negligible effects on R-LPS-induced splenomegaly, plasma antibody responses, liver inflammation, and inflammation-associated kidney gene expression. Collectively, our results show for the first time that absence of O-antigenic polysaccharide in R-LPS is critical to accelerated GN in lupus-prone mice. Furthermore, intervention by lipidome modulation through DHA feeding or sEH inhibition suppressed R-LPS-induced GN; however, these ameliorative effects were greatly diminished upon combining the treatments.

opencc-zeroDec 2022View details →

zenodo36/100

Lipidomics for diagnosis and prognosis of pulmonary hypertension

Pulmonary hypertension (PH) is associated with high morbidity and mortality with an urgent need for diagnostic and prognostic biomarkers. A training cohort of PH patients, disease controls without PH, and healthy controls was investigated using metabolomics and machine learning. Specific free fatty acid (FFA)/lipid-ratio biomarkers were diagnostic and predictive for PH survival with an area under the curve (AUC) of 0.89. FFA/lipid-ratio performance was independently validated in PH patients from other centers(AUC 0.90). Survival could be predicted in an age-independent manner and a combination with established clinical scores (FPHR4p, COMPERA 2.0) increased the scores hazard risk. Our mechanistic studies in healthy and diseased pulmonary artery endothelial and smooth muscle cells indicate a functional involvement of increased FFA levels in pathophysiology of PH. In conclusion, lipidomic changes in PH can be used as a novel diagnostic and prognostic approach and may help the discovery of new therapeutic targets.

opencc-by-4.0Apr 2023View details →

zenodo36/100

Lipidomics of mitochondria isolated from human fibroblasts

Mitochondrial trifunctional protein (TFP) has a monolysocardiolipin-acyltransferase (MLCL-AT) activity and therefore establishes a link between fatty acid oxidation and cardiolipin remodelling. We hypothesized that TFP deficiency produced changes in cardiolipin and other phospholipid content and composition in mitochondria of TFP cultured fibroblasts. The data showed that phospholipid profiles varied among patient fibroblasts. There was a correlation between genotype and the phospholipid profiles. Two profiles were found when cardiolipin, monolysocardiolipin, and oxidized cardiolipin and other phospholipids were considered, one of them similar to Barth syndrome. We concluded that cardiolipin remodeling may play a role in the pathogenesis of at least some patients with TFP/LCHAD deficiency. A previously described protocol was employed for the identification and quantification of mitochondrial phospholipids (including CL) and oxidized phospholipids by LC-MS/MS [1]. Briefly, lipids were extracted using the Folch method, total phosphate content was quantified, and samples were then analyzed using a LC-MS/MS system. The identification and quantification of the lipid species were achieved with an optimized workflow using SIEVE 2.2 software, and an in-house database. [1]. Chao H, Anthonymuthu TS, Kenny EM, Amoscato AA, Cole LK, Hatch GM et al. Disentangling oxidation/hydrolysis reactions of brain mitochondrial cardiolipins in pathogenesis of traumatic injury. JCI Insight 2018;3(21).

opencc-by-4.0Dec 2022View details →

dryad36/100

Lipidomic data of macrophages isolated from adult fruit flies (Drosophila melanogaster) 24 hours post-infection

The immune response is an energy-demanding process that must be coordinated with systemic metabolic changes redirecting nutrients from stores to the immune system. Although this interplay is fundamental for the function of the immune system, the underlying mechanisms remain elusive. Our data show that the pro-inflammatory polarization of Drosophila macrophages is coupled to the production of the insulin antagonist ImpL2 through the activity of the transcription factor HIF1α. ImpL2 production, reflecting nutritional demands of activated macrophages, subsequently impairs insulin signaling in the fat body, thereby triggering FOXO-driven mobilization of lipoproteins. This metabolic adaptation is fundamental for the function of the immune system and an individual's resistance to infection. We demonstrated that analogically to Drosophila, mammalian immune-activated macrophages produce ImpL2 homolog IGFBP7 in a HIF1α-dependent manner and that enhanced IGFBP7 production by these cells induces mobilization of lipoproteins from hepatocytes. Hence, the production of ImpL2/IGFBP7 by macrophages represents an evolutionarily conserved mechanism by which macrophages alleviate insulin signaling in the central metabolic organ to secure nutrients necessary for their function upon bacterial infection.

opencc-zeroSep 2023View details →

dryad36/100

Lipidomic profiling of SPNS1-KO lysosomes

Lysosomes degrade macromolecules and recycle their nutrient content to support cell function and survival. Yet, the machineries involved in lysosomal recycling of many nutrients remain to be discovered, with a notable example being choline, an essential metabolite liberated via phospholipid degradation. Here, we engineered metabolic dependency on lysosome-derived choline in pancreatic cancer cells to perform an endolysosome-focused CRISPR-Cas9 screen for genes mediating lysosomal choline recycling. We identified the orphan lysosomal transmembrane protein SPNS1 as critical for cell survival under choline limitation. SPNS1 loss leads to intralysosomal accumulation of lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE). Mechanistically, we reveal that SPNS1 is a proton gradient-dependent transporter of LPC species from the lysosome for their re-esterification into phosphatidylcholine in the cytosol. Finally, we establish that LPC efflux by SPNS1 is required for cell survival under choline limitation. Collectively, our work defines a lysosomal phospholipid salvage pathway that is essential under nutrient limitation, and more broadly, provides a robust platform to deorphan lysosomal gene function.

opencc-zeroSep 2023View details →

dryad36/100