Similar Datasets
Project description:Metabolomics studies of human plasma demonstrate a correlation of lower plasma lysophosphatidylcholines (LPC) concentrations with insulin resistance, obesity, and inflammation. This relationship is not unraveled on a molecular level. Here we investigated the effects of the abundant LPC(16:0) and LPC(18:1) on human skeletal muscle cells differentiated to myotubes. Transcriptome analysis of human myotubes treated with 10 µM LPC for 24 h revealed enrichment of up-regulated peroxisome proliferator-activated receptor (PPAR) target transcripts, including ANGPTL4, PDK4, PLIN2, and CPT1A. The increase in both PDK4 and ANGPTL4 RNA expression was abolished in the presence of either PPARδ antagonist GSK0660 or GSK3787. The induction of PDK4 by LPCs was blocked with siRNA against PPARD. The activation of PPARδ transcriptional activity by LPC was shown as PPARδ-dependent luciferase reporter gene expression and enhanced DNA binding of the PPARδ/RXR dimer. On a functional level, further results show that the LPC-mediated activation of PPARδ can reduce fatty acid-induced inflammation and ER stress in human skeletal muscle cells. The protective effect of LPC was prevented in the presence of the PPARδ antagonist GSK0660. Taking together, LPCs can activate PPARδ, which is consistent with the association of high plasma LPC levels and PPARδ-dependent anti-diabetic and anti-inflammatory effects.
2016-10-14 | GSE77337 | GEO
Project description:A transcriptomic meta-analysis of over 400 microarrays was undertaken to compare LPC lines against datasets of; muscle and embryonic stem cell lines, embryonic and developed liver (DL), and HCC. Uploaded here, is the array data from seven of the ten LPC lines used. These seven were prepared in our laboratory. The remaining LPC arrays and arrays from other tissues/cells were obtained from the GEO. A total of 405 microarrays were analysed in a meta analysis. This included the 381 publically-sourced arrays (13 of which were LPC arrays) and 24 LPC arrays performed within our lab. This data was mined to obtain signature LPC pathways and novel markers.
2016-08-03 | E-GEOD-85114 | biostudies-arrayexpress
Project description:Lysophosphatidylcholines (LPCs) are potent bioactive lipids whose fatty acid composition dictates their immunomodulatory effects. Here, we delineate how unsaturated LPC 18:2 and saturated LPC 16:0 differentially regulate neutrophil survival and inflammatory programs. LPC 18:2 markedly increased reactive oxygen species (ROS) generation and caspase-3/7 activation, accompanied by Annexin V positivity, mitochondrial membrane depolarization, and cytochrome C release, f. Features consistent with intrinsic apoptosis. In contrast, LPC 16:0 induced robust LDH and HMGB-1 release, indicating membrane rupture and pyroptosis-like death. Bulk RNA sequencing revealed that LPC 16:0 strongly upregulated inflammatory and cytokine genes. Disruption of lipid-raft integrity abolished LPC 18:2–induced ROS and apoptosis, underscoring the dependence of these effects on membrane organization. Collectively, these results identify LPC 18:2 as a non-inflammatory, mitochondria-dependent inducer of neutrophil apoptosis, whereas LPC 16:0 promotes inflammatory, lytic death programs. These findings highlight how lipid saturation determines neutrophil fate and immune tone, providing mechanistic insight into how distinct LPC species shape inflammation and tissue injury.
2026-02-13 | GSE311051 | GEO
Project description:This study investigated the effect of Vagus Nerve Stimulation (VNS) on innate neuroinflammation and remyelination in lysolecithin (LPC) induced demyelination, a preclinical model for Multiple Sclerosis (MS). In a first experiment (demyelination experiment), LPC was injected in the corpus callosum of 33 Lewis rats, inducing a demyelinated lesion, and rats were treated with either continuously-cycled VNS (cVNS) or one-minute per day VNS (1minVNS) or sham VNS, from two days before the injection until three days post-injection (dpi), when they were killed for immunohistochemistry and proteomics analysis. This timepoint corresponded with a demyelinated lesion and peak inflammation. In a second experiment (remyelination experiment), 13 rats were analogously treated with either cVNS or sham from two days before LPC injection until 11 dpi, when they were killed for tissue prelevation for immunohistochemistry and proteomics. This timepoints corresponded with partial remyelination of the lesion. For proteomics analysis, 20 rats were randomly selected, namely five cVNS and five sham rats of the demyelination experiment, and five cVNS and five sham rats of the remyelination experiment.
2024-05-10 | PXD050858 | Pride
Project description:To assess the preclinical Aldara model, the proteomic response of mouse skin to topical applied Aldara cream was assessed using untargeted LC-MS. Skin from sham treated or treated with the Aldara cream were compared for 4 independent experiments after 8 days of treatment.
2025-04-22 | PXD056245 | Pride
Project description:We compared the transcriptomic responses in the mouse white matter tissue drive white matter lesions following LPC- and L-NIO-induced injury.
2025-12-08 | GSE312001 | GEO