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Journal of Oleo Science 2015Lysophosphatidylcholine (LPC) is amphiphilic substance, and possesses excellent physiological functions. In this study, LPC was prepared through ethanolysis of...
Lysophosphatidylcholine (LPC) is amphiphilic substance, and possesses excellent physiological functions. In this study, LPC was prepared through ethanolysis of phosphatidylcholine (PC) in n-hexane or solvent free media catalyzed by Novozym 435 (from Candida antarctica), Lipozyme TLIM (from Thermomcyces lanuginosus) and Lipozyme RMIM (from Rhizomucor miehei). The results showed that three immobilized lipases from Candida Antarctica, Thermomcyces lanuginosus and Rhizomucor miehei could catalyze ethanolysis of PC efficiently. In n-hexane, the LPC conversions of ethanolysis of PC catalyzed by Novozyme 435, Lipozyme TLIM and Lipozyme RMIM could reach to 98.5 ± 1.6%, 94.6 ± 1.4% and 93.7 ± 1.8%, respectively. In solvent free media, the highest LPC conversions of ethanolysis of PC catalyzed by Novozyme 435, Lipozyme TL IM and Lipozyme RM IM were 97.7 ± 1.7%, 93.5 ± 1.2% and 93.8 ± 1.9%, respectively. The catalytic efficiencies of the three lipases were in the order of Novozyme 435 > Lipozyme TLIM > Lipozyme RMIM. Furthermore, their catalytic efficiencies in n-hexane were better than those in solvent free media.
Topics: Azo Compounds; Biocatalysis; Enzymes, Immobilized; Ethanol; Fungal Proteins; Hexanes; Lipase; Lysophosphatidylcholines; Naphthalenes; Phosphatidylcholines; Surface-Active Agents
PubMed: 25766935
DOI: 10.5650/jos.ess14246 -
Scientific Reports Nov 2022Lysophosphatidylcholine (LPC) was previously found to show neuroprotective effect on nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) induced...
Lysophosphatidylcholine (LPC) was previously found to show neuroprotective effect on nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) induced signalings. Also, numerous studies reported the emerging roles of long noncoding RNAs (LncRNAs) involved in neurodegenerative disease. However, the biological mechanism of LPC and expression profile of lncRNAs has not been reported. Here, lncRNAs in PC12 cells under LPC and NGF treatment were analyzed using high throughput sequencing technology for the first time. We identified 564 annotated and 1077 novel lncRNAs in PC12 cells. Among them, 121 lncRNAs were differentially expressed in the PC12 cells under LPC stimulation. KEGG analysis showed that differentially expressed mRNAs co-expressed with lncRNAs mainly enriched in ribosome, oxidative phosphorylation, Parkinson's disease, Huntington's disease and Alzheimer's disease etc. LncRNA-mRNA network analysis showed that lncRNA ENSRNOT00000082515 had interactions with 626 different mRNAs suggesting that lncRNA ENSRNOT00000082515 probably play vital role. Finally, sequencing data were validated by qRT-PCR for ENSRNOT00000084874, ENSRNOT00000082515, LNC_001033 forward Fgf18, Vcam1, and Pck2.
Topics: Rats; Animals; RNA, Long Noncoding; RNA, Messenger; Lysophosphatidylcholines; Nerve Growth Factor; Gene Expression Profiling; PC12 Cells; Neurodegenerative Diseases; Gene Regulatory Networks
PubMed: 36369435
DOI: 10.1038/s41598-022-21676-5 -
Pathophysiology of Haemostasis and... 2006Oxidation of low-density lipoprotein (LDL) generates pro-inflammatory and pro-thrombotic mediators that play a crucial role in cardiovascular and inflammatory diseases.... (Review)
Review
Oxidation of low-density lipoprotein (LDL) generates pro-inflammatory and pro-thrombotic mediators that play a crucial role in cardiovascular and inflammatory diseases. Mildly oxidized LDL (mox-LDL) and minimally modified LDL (mm-LDL) which escape the uptake of macrophage scavenger receptors accumulate in the atherosclerotic intima. Oxidatively modified LDL is also present within the electronegative LDL fraction in blood, which is elevated in patients at high risk for cardiovascular diseases. Mox-LDL and mm-LDL, but not native LDL are able to induce platelet shape change and aggregation. LDL oxidation generates lipids with platelet stimulatory properties such as lysophosphatidylcholine, certain oxidized phosphatidylcholine molecules, F(2)-isoprostanes and lysophosphatidic acid (LPA). Mox-LDL and mm-LDL are like a Trojan horse carrying these biologically active lipids and attacking cells through activation of physiological receptors and signaling mechanisms. LPA has been identified as the lipid responsible for platelet stimulation by mox-LDL, mm-LDL and also mox-HDL. These lipoproteins activate platelets by stimulating G-protein coupled LPA receptors and a Rho/Rho kinase signaling pathway leading to platelet shape change and subsequent aggregation. LPA-mediated platelet activation might contribute to arterial thrombus formation after rupture of atherosclerotic plaques and to the increased blood thrombogenicity of patients with cardiovascular diseases.
Topics: Blood Coagulation; Blood Platelets; Cholesterol, LDL; F2-Isoprostanes; Fibrinolysis; Humans; Lipids; Lysophosphatidylcholines; Lysophospholipids; Oxidation-Reduction; Phosphatidylcholines; Platelet Activation; Signal Transduction
PubMed: 16877878
DOI: 10.1159/000093222 -
International Journal of Molecular... Jun 2020Lysophosphatidylcholines are a group of bioactive lipids heavily investigated in the context of inflammation and atherosclerosis development. While present in plasma... (Review)
Review
Lysophosphatidylcholines are a group of bioactive lipids heavily investigated in the context of inflammation and atherosclerosis development. While present in plasma during physiological conditions, their concentration can drastically increase in certain inflammatory states. Lysophosphatidylcholines are widely regarded as potent pro-inflammatory and deleterious mediators, but an increasing number of more recent studies show multiple beneficial properties under various pathological conditions. Many of the discrepancies in the published studies are due to the investigation of different species or mixtures of lysophatidylcholines and the use of supra-physiological concentrations in the absence of serum or other carrier proteins. Furthermore, interpretation of the results is complicated by the rapid metabolism of lysophosphatidylcholine (LPC) in cells and tissues to pro-inflammatory lysophosphatidic acid. Interestingly, most of the recent studies, in contrast to older studies, found lower LPC plasma levels associated with unfavorable disease outcomes. Being the most abundant lysophospholipid in plasma, it is of utmost importance to understand its physiological functions and shed light on the discordant literature connected to its research. LPCs should be recognized as important homeostatic mediators involved in all stages of vascular inflammation. In this review, we want to point out potential pro- and anti-inflammatory activities of lysophospholipids in the vascular system and highlight recent discoveries about the effect of lysophosphatidylcholines on immune cells at the endothelial vascular interface. We will also look at their potential clinical application as biomarkers.
Topics: Animals; Anti-Inflammatory Agents; Biomarkers; Humans; Inflammation; Inflammation Mediators; Lysophosphatidylcholines; Vascular Diseases
PubMed: 32599910
DOI: 10.3390/ijms21124501 -
Purinergic Signalling Sep 2022Even though macrophages have the potential to harm tissues through excessive release of inflammatory mediators, they play protective roles to maintain tissue integrity....
Even though macrophages have the potential to harm tissues through excessive release of inflammatory mediators, they play protective roles to maintain tissue integrity. In this study, we hypothesized that lysophosphatidylcholine (LPC), via G2A and A receptors, puts brakes on macrophages by the induction of adenosine release which could contribute to termination of inflammation. Mechanistically, LPC-induced PGE production followed by the activation of cAMP/protein kinase A (PKA) pathway which results in the activation of LKB1/AMPK signaling pathway leading to increasing Mg influx concomitantly with an increase in mitochondrial membrane potential (MMP, Δψ) and ATP production. Then, ATP is converted to adenosine intracellularly followed by efflux via ENT1. In a parallel pathway, LPC-induced elevation of cytosolic calcium was essential for adenosine release, and Ca/calmodulin signaling cooperated with PKA to regulate ENT1 permeation to adenosine. Pharmacological blockade of TRPM7 and antisense treatment suppressed LPC-induced adenosine release and magnesium influx in bone marrow-derived macrophages (BMDMs). Moreover, LPC suppressed LPS-induced phosphorylation of connexin-43, which may counteract TLR4-mediated inflammatory response. Intriguingly, we found LPC increased netrin-1 production from BMDMs. Netrin-1 induces anti-inflammatory signaling via A receptor. In the presence of adenosine deaminase which removes adenosine in the medium, the chemotaxis of macrophages toward LPC was significantly increased. Hypoxia and metabolic acidosis are usually developed in a variety of inflammatory situations such as sepsis. We found LPC augmented hypoxia- or acidosis-induced adenosine release from BMDMs. These results provide evidence of LPC-induced brake-like action on macrophages by adenosine release via cellular magnesium signaling.
Topics: Adenosine; Adenosine Triphosphate; Cyclic AMP-Dependent Protein Kinases; Hypoxia; Lysophosphatidylcholines; Macrophages; Magnesium; Netrin-1; Protein Serine-Threonine Kinases; TRPM Cation Channels
PubMed: 35779163
DOI: 10.1007/s11302-022-09878-y -
Fukushima Journal of Medical Science Jun 2016We compared the effects of lysophosphatidylcholine (LPC) and acetylcholine (ACh) on IK(ACh), ICa and a non-selective cation current (INSC) in guinea-pig atrial myocytes...
We compared the effects of lysophosphatidylcholine (LPC) and acetylcholine (ACh) on IK(ACh), ICa and a non-selective cation current (INSC) in guinea-pig atrial myocytes to clarify whether LPC and ACh activate similar Gi/o-coupled effector systems. IK(ACh), ICa and INSC were analyzed in single atrial myocytes by the whole cell patch-clamp. LPC induced INSC in a concentration-dependent manner in atrial cells. ACh activated IK(ACh), but failed to evoke INSC. LPC also activated IK(ACh) but with significantly less potency than ACh. The effects of both ligands on IK(ACh) were inhibited by intracellular loading of pre-activated PTX. This treatment also inhibited LPC-induced INSC, indicating that IK(ACh) and INSC induced by LPC are both mediated by Gi/o. LPC and ACh had similar potencies in inhibiting ICa, which was pre-augmented by forskolin, indicating that LPC and ACh activate similar amounts of α-subunits of Gi/o. The different effects of LPC and ACh on IK(ACh) and INSC may suggest that LPC and ACh activate Gi/o having different types of βγ subunits, and that LPC-induced INSC may be mediated by βγ subunits of Gi/o, which are less effective in inducing IK(ACh).
Topics: Acetylcholine; Animals; Calcium Channels, L-Type; Colforsin; Guinea Pigs; Heart Atria; Lysophosphatidylcholines; Male; Membrane Potentials; Myocytes, Cardiac; Pertussis Toxin; Potassium Channels
PubMed: 26911304
DOI: 10.5387/fms.2015-23 -
Bioscience Reports Oct 2022Although metabolomic analysis for patients with nonalcoholic fatty liver disease (NAFLD) was a promising approach to identify novel biomarkers as targets for the...
BACKGROUND
Although metabolomic analysis for patients with nonalcoholic fatty liver disease (NAFLD) was a promising approach to identify novel biomarkers as targets for the diagnosis of NAFLD, the serum metabolomics profile of early-stage NAFLD patients from central China remain unknown.
OBJECTIVE
The aim of the present study was to explore the metabolic characteristics of patients with early-stage NAFLD based on the ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) technology, to identify differential metabolites and perform functional analysis, and especially, to establish a novel early NAFLD clinical diagnostic tool.
RESULTS
Compared with healthy controls, serum metabolite species increased significantly in early stage NAFLD patients. Expression of 88 metabolites including 1-naphthylmethanol, rosavin, and theophylline were up-regulated in early NAFLD, while 68 metabolites including 2-hydroxyphenylacetic acid and lysophosphatidylcholine (24:1(15Z)) were down-regulated. The early NAFLD classifier achieved a strong diagnostic efficiency in the discovery phases (80.99%) and was successfully verified in the validation phases (75.23%).
CONCLUSIONS
These results advance our understanding about the composition and biological functions of serum metabolites of early NAFLD. In addition, serum metabolic markers can serve as an efficient diagnostic tool for the early-stage NAFLD.
Topics: Humans; Non-alcoholic Fatty Liver Disease; Chromatography, Liquid; Lysophosphatidylcholines; Theophylline; Tandem Mass Spectrometry; Metabolome; Metabolomics; Biomarkers
PubMed: 36124945
DOI: 10.1042/BSR20220319 -
International Journal of Molecular... May 2021Insulin plays a significant role in carbohydrate homeostasis as the blood glucose lowering hormone. Glucose-induced insulin secretion (GSIS) is augmented by...
Insulin plays a significant role in carbohydrate homeostasis as the blood glucose lowering hormone. Glucose-induced insulin secretion (GSIS) is augmented by glucagon-like peptide (GLP-1), a gastrointestinal peptide released in response to ingesting nutriments. The secretion of insulin and GLP-1 is mediated by the binding of nutrients to G protein-coupled receptors (GPCRs) expressed by pancreatic β-cells and enteroendocrine cells, respectively. Therefore, insulin secretagogues and incretin mimetics currently serve as antidiabetic treatments. This study demonstrates the potency of synthetic isoprenoid derivatives of lysophosphatidylcholines (LPCs) to stimulate GSIS and GLP-1 release. Murine insulinoma cell line (MIN6) and enteroendocrinal L cells (GLUTag) were incubated with LPCs bearing geranic acid (1-GA-LPC), citronellic acid (1-CA-LPC), 3,7-dimethyl-3-vinyloct-6-enoic acid (GERA-LPC), and (E)-3,7,11-trimethyl- 3-vinyldodeca-6,10-dienoic acid (1-FARA-LPC). Respective free terpene acids were also tested for comparison. Besides their insulin- and GLP-1-secreting capabilities, we also investigated the cytotoxicity of tested compounds, the ability to intracellular calcium ion mobilization, and targeted GPCRs involved in maintaining lipid and carbohydrate homeostasis. We observed the high cytotoxicity of 1-GERA-LPC and 1-FARA-LPC in contrast 1-CA-LPC and 1-GA-LPC. Moreover, 1-CA-LPC and 1-GA-LPC demonstrated the stimulatory effect on GSIS and 1-CA-LPC augmented GLP-1 secretion. Insulin and GLP-1 release appeared to be GPR40-, GPR55-, GPR119- and GPR120-dependent.
Topics: Calcium; Glucagon-Like Peptide 1; Humans; Insulin; Insulin Secretion; Intracellular Space; Lipid Metabolism; Lysophosphatidylcholines; Molecular Structure; Receptors, G-Protein-Coupled; Terpenes
PubMed: 34072220
DOI: 10.3390/ijms22115748 -
GeroScience Aug 2022Lysophosphatidylcholines (LPCs) are phospholipids critical in the synthesis of cardiolipin, an essential component of mitochondrial membranes. Lower plasma LPCs have...
Lysophosphatidylcholines (LPCs) are phospholipids critical in the synthesis of cardiolipin, an essential component of mitochondrial membranes. Lower plasma LPCs have been cross-sectionally associated with lower skeletal muscle mitochondrial function, but whether lower LPCs and their decline over time are longitudinally associated with an accelerated decline of mitochondria function is unknown. We analyzed data from 184 participants in the Baltimore Longitudinal Study of Aging (mean age: 74.5 years, 57% women, 25% black) who had repeated measures of plasma LPCs (16:0, 16:1, 17:0, 18:0, 18:1, 18:2, 20:3, 20:4, 24:0, and 28:1) by liquid chromatography-tandem mass spectrometry and repeated measures of skeletal muscle oxidative capacity (k) assessed by P magnetic resonance spectroscopy over an average of 2.4 years. Rates of change in k and each LPC were first estimated using simple linear regression. In multivariable linear regression models adjusted for baseline demographics and PCr % depletion, lower baseline LPC 16:1 and faster rates of decline in LPC 16:1 and 18:1 were significantly associated with a faster rate of decline in k (B = - 0.169, 95% CI: - 0.328, - 0.010, p = 0.038; B = 0.209, 95% CI: 0.065, 0.352, p = 0.005; B = 0.156, 95% CI: 0.011, 0.301, p = 0.035, respectively). Rates of change in other LPCs were not significantly associated with change in k (all p > 0.05). Lower baseline concentrations and faster decline in selected plasma lysophosphatidylcholines over time are associated with faster decline in skeletal muscle mitochondrial function. Strategies to prevent the decline of plasma LPCs at an early stage may slow down mitochondrial function decline and impairment during aging.
Topics: Humans; Female; Aged; Male; Lysophosphatidylcholines; Longitudinal Studies; Muscle, Skeletal; Mitochondria; Aging
PubMed: 35389191
DOI: 10.1007/s11357-022-00548-w -
Journal of Lipid Research Nov 1993The role of the lysosome in the metabolism of lysophosphatidylcholine was investigated in isolated rat hepatocytes. Chloroquine, primaquine, and ammonium chloride caused...
The role of the lysosome in the metabolism of lysophosphatidylcholine was investigated in isolated rat hepatocytes. Chloroquine, primaquine, and ammonium chloride caused a 2.5-fold increase in radioactive lysophosphatidylcholine in [methyl-3H]choline-labeled cells. This effect was confirmed by a 1.7-fold increase in lysophosphatidylcholine mass in chloroquine-treated hepatocytes. Chloroquine caused a 2.7-fold increase in radioactive lysophosphatidylethanolamine in [1-3H]ethanolamine-labeled cells and a 2.3-fold increase in radioactive lysophosphatidylcholine in [methyl-3H]methionine-labeled cells. Chloroquine did not affect formation of choline-containing aqueous metabolites or the level of radioactivity in phosphatidylcholine (PC). The effect of chloroquine on radioactive lysophosphatidylcholine accumulation was concentration-dependent and occurred within 10 min, consistent with rapid inhibition of lysosomal function. As there was no observed decrease in the 3H in PC, the accumulation of lysophosphatidylcholine was likely due to the inhibition of acid lysophospholipase activity in chloroquine-treated cells. The accumulation of lysophosphatidylcholine in the presence of chloroquine was observed in both short-term- (30 min) and equilibrium-(24 h) [methyl-3H]choline-labeled cells. Simultaneous incubation of hepatocytes with both albumin and chloroquine increased the radioactivity in lysophosphatidylcholine in the medium independently of the accumulation of radioactive lysophosphatidylcholine in the cells. The results suggest that there are separate pools of lysophosphatidylcholine in the hepatocyte and that the pool donated to an extracellular acceptor is different from the lysosomal pool.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Albumins; Animals; Brefeldin A; Chloroquine; Choline; Cyclopentanes; Cytidine Diphosphate Choline; Liver; Lysophosphatidylcholines; Lysosomes; Methionine; Methylation; Phosphatidylcholines; Rats; Tritium
PubMed: 8263412
DOI: No ID Found