Artículos de revistas: "LysoPAF"

1

Chai, Yuh-Cherng, David G. Binion y Guy M. Chisolm. "Relationship of molecular structure to the mechanism of lysophospholipid-induced smooth muscle cell proliferation". American Journal of Physiology-Heart and Circulatory Physiology 279, n.º 4 (1 de octubre de 2000): H1830—H1838. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1830.

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We previously reported that oxidized low-density lipoprotein and one of its constituents, lysophosphatidylcholine (lysoPC), caused smooth muscle cell proliferation that was inhibitable by vitamin E and by a neutralizing antibody against basic fibroblast growth factor-2 (FGF-2). We now show that the mitogenic activity of lysolipids is highly dependent on structure. Phospholipids with palmitoyl fatty acid and phosphocholine induced DNA synthesis optimally. Shorter and longer fatty acids were significantly less potent, as were phosphoserine and phosphoethanolamine head groups. Structurally related phospholipids [platelet-activating factor (PAF) and lysoPAF] were also mitogens and acted via an analogous FGF-2-dependent, vitamin E-inhibitable mechanism. The mechanism of lysoPC stimulation was distinct from that of another phospholipid mitogen, lysophosphatidic acid (lysoPA), in that lysoPC stimulation was not pertussis toxin inhibitable. Furthermore, lysoPA stimulation was not inhibitable by vitamin E. Despite its distinct cellular pathway for stimulation, lysoPA also ultimately led to FGF-2 release. Our data show that specific structural attributes of lysoPC, PAF, and lysoPAF enable these agents to mediate smooth muscle cell release of FGF-2, which in turn stimulates proliferation.

2

Bakken, A. M. y M. Farstad. "The activities of acyl-CoA:1-acyl-lysophospholipid acyltransferase(s) in human platelets". Biochemical Journal 288, n.º 3 (15 de diciembre de 1992): 763–70. http://dx.doi.org/10.1042/bj2880763.

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The activities of acyl-CoA:1-acyl-lysophospholipid acyltransferases (EC 2.3.1.23) have been studied in human platelet lysates by using endogenously formed [14C]acyl-CoA from [14C]fatty acid, ATP and CoA in the presence of 1-acyl-lysophosphatidyl-choline (lysoPC), -ethanolamine (lysoPE), -serine (lysoPS) or -inositol (lysoPI). Linoleic acid as fatty acid substrate had the highest affinity to acyl-CoA:1-acyl-lysophospholipid acyltransferase with lysoPC as variable substrate, followed by eicosapentaenoic acid (EPA) and arachidonic acid (AA). The activity at optimal conditions was 7.4, 7.3 and 7.2 nmol/min per 10(9) platelets with lysoPC as substrate, with linoleic acid, AA and EPA respectively. EPA and AA were incorporated into all lyso-forms. Linoleic acid was also incorporated into lysoPE at a high rate, but less into lysoPS and lysoPI. DHA was incorporated into lysoPC and lysoPE, but only slightly into lysoPI and lysoPS. Whereas incorporation of all fatty acids tested was maximal for lysoPC and lysoPI at 200 and 80 microM respectively, maximal incorporation needed over 500 microM for lysoPE and lysoPS. The optimal concentration for [14C]fatty acid substrates was in the range 15-150 microM for all lysophospholipids. Competition experiments with equimolar concentrations of either lysoPC and lysoPI or lysoPE resulted in formation of [14C]PC almost as if lysoPI or lysoPE were not added to the assay medium.

3

Schindler, Peter W. y Ewa Ninio. "Kinetic studies of human and rat neutrophil lysoPAF acetyltransferase using lysoPAF and dansyllysoPAF as substrates". Lipids 26, n.º 12 (diciembre de 1991): 1004–10. http://dx.doi.org/10.1007/bf02536492.

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4

Thumser, A. E., J. E. Voysey y D. C. Wilton. "The binding of lysophospholipids to rat liver fatty acid-binding protein and albumin". Biochemical Journal 301, n.º 3 (1 de agosto de 1994): 801–6. http://dx.doi.org/10.1042/bj3010801.

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The binding of lysophospholipids to rat liver fatty acid-binding protein (FABP) and to BSA and human serum albumin was investigated by using competitive displacement fluorescence assays by monitoring the displacement of the fluorescent fatty acid probe 11-(dansylamino)undecanoic acid (DAUDA). In addition, direct binding assays using changes in tryptophan fluorescence were possible with albumin. Liver FABP was able to bind a range of lysophospholipids, oleoyl-lysophosphatidic acid (lysoPA), oleoyl-lysophosphatidylcholine (lysoPC), oleoyl-lysophosphatidylethanolamine (lysoPE) and oleoyl-lysophosphatidylglycerol, with similar affinity and a Kd of about 1 microM. Liver FABP was also able to bind lysophospholipids generated by the action of phospholipase A2 or phospholipase A1 (triacylglycerol lipase) on phospholipid vesicles. A possible physiological role for liver FABP in lysophospholipid metabolism within the cell is discussed. Albumin was shown to bind lysoPA with higher affinity than either lysoPC or lysoPE, and the initial minimal DAUDA displacement by lysoPA indicated that lysoPA was binding to the primary high-affinity fatty acid-binding sites on albumin and that, like oleic acid, about 3 mol of ligand/mol was bound to these sites. Kd values in the microM range were indicated for lysoPC and lysoPE, whereas, by comparison with oleic acid, the Kd for lysoPA was significantly lower and high-affinity binding in the nM range was indicated. Overall, the data suggest that, because of structural similarity, lysoPA binds to albumin in a similar manner to long-chain fatty acids.

5

NAGUMO, Seiji, Akira FUKUJU, Mitsue TAKAYAMA, Masahiro NAGAI, Ryohei YANOSHITA y Yuji SAMEJIMA. "Inhibition of LysoPAF Acetyltransferase Activity by Components of Licorice Root." Biological & Pharmaceutical Bulletin 22, n.º 10 (1999): 1144–46. http://dx.doi.org/10.1248/bpb.22.1144.

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6

Aoyama, Chieko, Hiroyuki Sugimoto, Hiromi Ando, Satoko Yamashita, Yasuhiro Horibata, Sayaka Sugimoto y Motoyasu Satou. "The heterotrimeric G protein subunits Gαq and Gβ1 have lysophospholipase D activity". Biochemical Journal 440, n.º 2 (14 de noviembre de 2011): 241–50. http://dx.doi.org/10.1042/bj20110545.

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In a previous study we purified a novel lysoPLD (lysophospholipase D) which converts LPC (lysophosphatidylcholine) into a bioactive phospholipid, LPA (lysophosphatidic acid), from the rat brain. In the present study, we identified the purified 42 and 35 kDa proteins as the heterotrimeric G protein subunits Gαq and Gβ1 respectively. When FLAG-tagged Gαq or Gβ1 was expressed in cells and purified, significant lysoPLD activity was observed in the microsomal fractions. Levels of the hydrolysed product choline increased over time, and the Mg2+ dependency and substrate specificity of Gαq were similar to those of lysoPLD purified from the rat brain. Mutation of Gαq at amino acids Lys52, Thr186 or Asp205, residues that are predicted to interact with nucleotide phosphates or catalytic Mg2+, dramatically reduced lysoPLD activity. GTP does not compete with LPC for the lysoPLD activity, indicating that these substrate-binding sites are not identical. Whereas the enzyme activity of highly purified FLAG-tagged Gαq overexpressed in COS-7 cells was ~4 nmol/min per mg, the activity from Neuro2A cells was 137.4 nmol/min per mg. The calculated Km and Vmax values for lysoPAF (1-O-hexadecyl-sn-glycero-3-phosphocholine) obtained from Neuro2A cells were 21 μM and 0.16 μmol/min per mg respectively, similar to the enzyme purified from the rat brain. These results reveal a new function for Gαq and Gβ1 as an enzyme with lysoPLD activity. Tag-purified Gα11 also exhibited a high lysoPLD activity, but Gαi and Gαs did not. The lysoPLD activity of the Gα subunit is strictly dependent on its subfamily and might be important for cellular responses. However, treatment of Hepa-1 cells with Gαq and Gα11 siRNAs (small interfering RNAs) did not change lysoPLD activity in the microsomal fraction. Clarification of the physiological relevance of lysoPLD activity of these proteins will need further studies.

7

Guimbaud, Rosine, Angelo Izzo, Jean Pierre Martinolle, Nicole Vidon, Daniel Couturier, Jacques Benveniste y Stanislas Chaussade. "Intraluminal excretion of PAF, lysoPAF, and acetylhydrolase in patients with ulcerative colitis". Digestive Diseases and Sciences 40, n.º 12 (diciembre de 1995): 2635–40. http://dx.doi.org/10.1007/bf02220453.

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8

Christman, B. W., J. W. Christman, R. Dworski, I. A. Blair y C. Prakash. "Prostaglandin E2 limits arachidonic acid availability and inhibits leukotriene B4 synthesis in rat alveolar macrophages by a nonphospholipase A2 mechanism." Journal of Immunology 151, n.º 4 (15 de agosto de 1993): 2096–104. http://dx.doi.org/10.4049/jimmunol.151.4.2096.

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Abstract Prostaglandin E2 (PGE2), a potent mediator of inflammation released in large amounts by endotoxin-stimulated alveolar macrophages (AM), has been shown to inhibit leukotriene B4 (LTB4) release by activated neutrophils. We investigated the hypothesis that LTB4 synthesis by AM can be regulated by PGE2 and performed experiments to determine the biochemical site of regulation. AM obtained from Sprague-Dawley rats were preincubated with PGE2 before stimulation with the calcium ionophore A23187. LTB4, platelet-activating factor (PAF), lysoPAF, (AA), and 5-hydroxyeicosatetraenoic acid were isolated from AM cells and supernatants, then quantified by gas chromatography/electron capture negative ion mass spectrometry. Stimulated AM released 30.50 +/- 4.52 ng LTB4/10(6) cells and were inhibited by PGE2 in a dose dependent manner. PGE2 (1 microM) inhibited LTB4 synthesis by 37% and decreased release of both 5-hydroxyeicosatetraenoic acid and arachidonic acid by stimulated AM, but did not alter synthesis of PAF or lysoPAF. These mass measurements suggest that PGE2 does not affect the activity of phospholipase A2, PAF acetyltransferase, leukotriene A4 hydrolase. We conclude that PGE2 attenuates LTB4 production in alveolar macrophages by altering the activity of lipases other than phospholipase A2. PGE2-mediated inhibition of LTB4 synthesis by AM may regulate the initiation of lung inflammation.

9

Petsini, Filio, Agathi Ntzouvani, Maria Detopoulou, Vasiliki D. Papakonstantinou, Nick Kalogeropoulos, Elizabeth Fragopoulou, Tzortzis Nomikos, Meropi D. Kontogianni y Smaragdi Antonopoulou. "Consumption of Farmed Fish, Fed with an Olive-Pomace Enriched Diet, and Its Effect on the Inflammatory, Redox, and Platelet-Activating Factor Enzyme Profile of Apparently Healthy Adults: A Double-Blind Randomized Crossover Trial". Foods 11, n.º 14 (15 de julio de 2022): 2105. http://dx.doi.org/10.3390/foods11142105.

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A fish-rich diet has a beneficial effect on cardiovascular health. The platelet activating factor (PAF) is involved in the development of atherosclerosis, and in vitro results support the regulating action of bioactive nutrients on PAF metabolism. The purpose of this study is to examine whether the consumption of farmed fish fed with an olive-pomace enriched diet (EF) affects PAF metabolism and the markers of inflammation and oxidative stress compared to the consumption of conventionally fed farmed fish (CF). Thirty apparently healthy adults completed a randomized double-blind crossover trial, during which they consumed both CF and EF twice a week for 8 weeks with a six-week washout period in between. The activities of PAF acetylhydrolase (PAF-AH), lysoPAF acetyltransferase (lysoPAF-AT), DTT-insensitive CDP-choline: 1-alkyl-2-acetyl-sn-glycerol-choline-phosphotransferase (PAF-CPT) in leukocytes, and lipoprotein-associated phospholipase A2 (LpPLA2) in serum were determined. The quantities of interleukin-6 (IL-6), high sensitivity C-reactive protein (hsCRP), oxidized LDL (ox-LDL), thiobarbituric acid-reactive substances (TBARS), and glutathione peroxidase (GPx), as well as the serum oxidation, were also determined. Both types of fish exerted similar effects as there were no statistically significant differences between the two interventions except for an elevated PAF-CPT and reduced arachidonic acid (AA) in the red blood cell (RBC) membrane lipids after the EF intake.

10

Noris, Marina, Daniela Macconi, Vittorio Nanni, Mario Salmona, Marta Todeschini y Giuseppe Remuzzi. "Defective glomerular [3H]lysoPAF metabolism in the autologous phase of rabbit nephrotoxic nephritis". Kidney International 44, n.º 4 (octubre de 1993): 747–54. http://dx.doi.org/10.1038/ki.1993.309.

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11

Thumser, A. E. A. y D. C. Wilton. "The binding of natural and fluorescent lysophospholipids to wild-type and mutant rat liver fatty acid-binding protein and albumin". Biochemical Journal 307, n.º 1 (1 de abril de 1995): 305–11. http://dx.doi.org/10.1042/bj3070305.

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Rat liver fatty acid-binding protein (FABP) is able to bind a wide range of non-polar anionic ligands, including lysophospholipids. In order to understand the nature of lysophospholipid interactions with liver FABP, the binding of natural lysophospholipids and two fluorescent analogues, N-(5-dimethylaminonaphthalenesulphonyl)-1-palmitoyl-sn-glycero-3- phosphoethanolamine (dansyl lysoPE) and 1-(O-[11-(5-dimethylaminonaphthalene-sulphonyl)amino]undecyl)-sn-glycero -3- phosphocholine (dansyl-C11-lysoPAF), has been investigated. The results confirmed the ability of liver FABP to bind lysophospholipids with KD values in the range of 1-2 microM, and a 1:1 binding stoichiometry was indicated. Binding of fluorescent lysophospholipids was enhanced with the FABP mutant, R122Q, possibly due to increased flexibility of the binding cavity as a result of reduced hydrogen-bonding constraints. The fluorescent lysophospholipids also bound to albumin, with KD values in the range 0.1-1.0 microM, and could be displaced by oleic acid. The fluorescence characteristics of the dansyl lysophospholipid analogue dansyl-C11-lyso-PAF suggested that this probe binds to the same site(s) on albumin as the fluorescent fatty acid probe 11-(5-dimethylaminonaphthalene-sulphonylamino)-undecanoic acid (DAUDA).

12

Goracci, Gianfrancesco y Ermelinda Francescangeli. "Properties of PAF-synthesizing phosphocholinetransferase and evidence for lysoPAF acetyltransferase activity in rat brain". Lipids 26, n.º 12 (diciembre de 1991): 986–91. http://dx.doi.org/10.1007/bf02536489.

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13

Aïssa, J., H. Harran, M. Rabeau, S. Boucherie, H. Brouilhet y J. Benveniste. "Tissue Levels of Histamine, PAF-Acether and Lysopaf-Acether in Carrageenan-lnduced Granuloma in Rats". International Archives of Allergy and Immunology 110, n.º 2 (1996): 182–86. http://dx.doi.org/10.1159/000237285.

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14

Murari, M. P., R. Murari, S. Parthasarathy, C. A. Guy, V. V. Kumar, B. Malewicz y Wolfgang J. Baumann. "Lyso platelet activating factor (LysoPAF) and its enantiomer. Total synthesis and carbon-13 NMR spectroscopy". Lipids 25, n.º 10 (octubre de 1990): 606–12. http://dx.doi.org/10.1007/bf02536010.

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15

Doebber, Thomas W., Margaret S. Wu, Anthony Mauriello y Alfred Alberts. "Platelet-activating factor (PAF) stimulates the lysoPAF acetyltransferase in leukocyte-rich plasma: Use in PAF antagonist studies". Lipids 26, n.º 12 (diciembre de 1991): 997–1003. http://dx.doi.org/10.1007/bf02536491.

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16

Flasiński, Michał, Paweł Wydro, Katarzyna Hąc-Wydro y Patrycja Dynarowicz-Łątka. "Cholesterol as a factor regulating the influence of natural (PAF and lysoPAF) vs synthetic (ED) ether lipids on model lipid membranes". Biochimica et Biophysica Acta (BBA) - Biomembranes 1828, n.º 11 (noviembre de 2013): 2700–2708. http://dx.doi.org/10.1016/j.bbamem.2013.07.024.

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17

SUN, Yong-Xin, Kazuhito TSUBOI, Yasuo OKAMOTO, Takeharu TONAI, Makoto MURAKAMI, Ichiro KUDO y Natsuo UEDA. "Biosynthesis of anandamide and N-palmitoylethanolamine by sequential actions of phospholipase A2 and lysophospholipase D". Biochemical Journal 380, n.º 3 (15 de junio de 2004): 749–56. http://dx.doi.org/10.1042/bj20040031.

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Anandamide (an endocannabinoid) and other bioactive long-chain NAEs (N-acylethanolamines) are formed by direct release from N-acyl-PE (N-acyl-phosphatidylethanolamine) by a PLD (phospholipase D). However, the possible presence of a two-step pathway from N-acyl-PE has also been suggested previously, which comprises (1) the hydrolysis of N-acyl-PE to N-acyl-lysoPE by PLA1/PLA2 enzyme(s) and (2) the release of NAEs from N-acyllysoPE by lysoPLD (lysophospholipase D) enzyme(s). In the present study we report for the first time the characterization of enzymes responsible for this pathway. The PLA1/PLA2 activity for N-palmitoyl-PE was found in various rat tissues, with the highest activity in the stomach. This stomach enzyme was identified as group IB sPLA2 (secretory PLA2), and its product was determined as N-acyl-1-acyl-lysoPE. Recombinant group IB, IIA and V of sPLA2s were also active with N-palmitoyl-PE, whereas group X sPLA2 and cytosolic PLA2α were inactive. In addition, we found wide distribution of lysoPLD activity generating N-palmitoylethanolamine from N-palmitoyl-lysoPE in rat tissues, with higher activities in the brain and testis. Based on several lines of enzymological evidence, the lysoPLD enzyme could be distinct from the known N-acyl-PE-hydrolysing PLD. sPLA2-IB dose dependently enhanced the production of N-palmitoylethanolamine from N-palmitoyl-PE in the brain homogenate showing the lysoPLD activity. N-Arachidonoyl-PE and N-arachidonoyl-lysoPE as anandamide precursors were also good substrates of sPLA2-IB and the lysoPLD respectively. These results suggest that the sequential actions of PLA2 and lysoPLD may constitute another biosynthetic pathway for NAEs, including anandamide.

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Sun, Han-Li y Tao Jiang. "The structure of nerve growth factor in complex with lysophosphatidylinositol". Acta Crystallographica Section F Structural Biology Communications 71, n.º 7 (27 de junio de 2015): 906–12. http://dx.doi.org/10.1107/s2053230x15008870.

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Nerve growth factor (NGF) is an important protein that is involved in a variety of physiological processes in cell survival, differentiation, proliferation and maintenance. The previously reported crystal structure of mouse NGF (mNGF) in complex with lysophosphatidylserine (LysoPS) showed that mNGF can bind LysoPS at its dimeric interface. To expand the understanding of the structural basis for specific lipid recognition by NGF, the crystal structure of mNGF complexed with lysophosphatidylinositol (13:0 LysoPI) was solved. Interestingly, in addition to Lys88, which interacts with the head glycerol group and the phosphate group of LysoPI, as seen in the mNGF–LysoPS structure, two additional residues, Tyr52 and Arg50, were found to assist in lipid binding by forming hydrogen bonds to the inositol moiety of the LysoPI molecule. The results suggest a specific recognition mechanism of inositol group-containing lipids by NGF, which may help in the design of bioactive compounds that can be delivered by NGF.

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Damnjanović, Jasmina, Hideo Nakano y Yugo Iwasaki. "Acyl chain that matters: introducing sn-2 acyl chain preference to a phospholipase D by protein engineering". Protein Engineering, Design and Selection 32, n.º 1 (enero de 2019): 1–11. http://dx.doi.org/10.1093/protein/gzz019.

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AbstractPhospholipase D (PLD) is an enzyme widely used for enzymatic synthesis of structured phospholipids (PLs) with modified head groups. These PLs are mainly used as food supplements and liposome ingredients. Still, there is a need for an enzyme that discriminates between PLs and lysoPLs, for specific detection of lysoPLs in various specimens and enzymatic synthesis of certain PLs from a mixed substrate. To meet this demand, we aimed at altering sn-2 acyl chain recognition of a PLD, leading to a variant enzyme preferably reacting on lysoPLs, by protein engineering. Based on the crystal structure of Streptomyces antibioticus PLD, W166 was targeted for saturation mutagenesis due to its strong interaction with the sn-2 acyl chain of the PL. Screening result pointed at W166R and W166K PLDs to selectively react on lysophosphatidylcholine (lysoPC), while not on PC. These variants showed a negative correlation between activity and sn-2 chain length of PL substrates. This behavior was not observed in the wild-type (WT)-PLD. Kinetic analysis revealed that the W166R and W166K variants have 7–10 times higher preference to lysoPC compared to the WT-PLD. Additionally, W166R PLD showed detectable activity toward glycero-3-phosphocholine, unlike the WT-PLD. Applicability of the lysoPC-preferring PLD was demonstrated by detection of lysoPC in the mixed PC/lysoPC sample and by the synthesis of cyclic phosphatidic acid. Structure model analyses supported the experimental findings and provided a basis for the structure model-based hypothesis on the observed behavior of the enzymes.

20

Sueajai, Jetjamnong, Nareerat Sutjarit, Nittaya Boonmuen, Saranya Auparakkitanon, Nantida Noumjad, Apichart Suksamrarn, Nawaporn Vinayavekhin y Pawinee Piyachaturawat. "Lowering of lysophosphatidylcholines in ovariectomized rats by Curcuma comosa". PLOS ONE 17, n.º 5 (19 de mayo de 2022): e0268179. http://dx.doi.org/10.1371/journal.pone.0268179.

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Decline of ovarian function in menopausal women increases metabolic disease risk. Curcuma comosa extract and its major compound, (3R)-1,7-diphenyl-(4E,6E)-4,6-heptadien-3-ol (DPHD), improved estrogen-deficient ovariectomized (OVX) rat metabolic disturbances. However, information on their effects on metabolites is limited. Here, we investigated the impacts of C. comosa ethanol extract and DPHD on 12-week-old OVX rat metabolic disturbances, emphasizing the less hydrophobic metabolites. Metabolomics analysis of OVX rat serum showed a marked increase compared to sham-operated rat (SHAM) in levels of lysophosphatidylcholines (lysoPCs), particularly lysoPC (18:0) and lysoPC (16:0), and of arachidonic acid (AA), metabolites associated with inflammation. OVX rat elevated lysoPCs and AA levels reverted to SHAM levels following treatments with C. comosa ethanol extract and DPHD. Overall, our studies demonstrate the effect of C. comosa extract in ameliorating the metabolic disturbances caused by ovariectomy, and the elevated levels of bioactive lipid metabolites, lysoPCs and AA, may serve as potential biomarkers of menopausal metabolic disturbances.

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Dyer, Kimberly D., Caroline M. Percopo, Zhihui Xie, Zhao Yang, John Dongil Kim, Francis Davoine, Paige Lacy, Kirk M. Druey, Redwan Moqbel y Helene F. Rosenberg. "Mouse and Human Eosinophils Degranulate in Response to Platelet-Activating Factor (PAF) and LysoPAF via a PAF-Receptor–Independent Mechanism: Evidence for a Novel Receptor". Journal of Immunology 184, n.º 11 (26 de abril de 2010): 6327–34. http://dx.doi.org/10.4049/jimmunol.0904043.

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22

Pei, Jiying, Shiguo Chen, Kefu Yu, Junjie Hu, Yitong Wang, Jingjing Zhang, Zhenjun Qin et al. "Metabolomics Characterization of Scleractinia Corals with Different Life-History Strategies: A Case Study about Pocillopora meandrina and Seriatopora hystrix in the South China Sea". Metabolites 12, n.º 11 (8 de noviembre de 2022): 1079. http://dx.doi.org/10.3390/metabo12111079.

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Life-history strategies play a critical role in susceptibility to environmental stresses for Scleractinia coral. Metabolomics, which is capable of determining the metabolic responses of biological systems to genetic and environmental changes, is competent for the characterization of species’ biological traits. In this study, two coral species (Pocillopora meandrina and Seriatopora hystrix in the South China Sea) with different life-history strategies (“competitive” and “weedy”) were targeted, and untargeted mass spectrometry metabolomics combined with molecular networking was applied to characterize their differential metabolic pathways. The results show that lyso-platelet activating factors (lyso-PAFs), diacylglyceryl carboxyhydroxymethylcholine (DGCC), aromatic amino acids, and sulfhydryl compounds were more enriched in P. meandrina, whereas new phospholipids, dehydrated phosphoglycerol dihydroceramide (de-PG DHC), monoacylglycerol (MAG), fatty acids (FA) (C < 18), short peptides, and guanidine compounds were more enriched in S. hystrix. The metabolic pathways involved immune response, energy metabolism, cellular membrane structure regulation, oxidative stress system, secondary metabolite synthesis, etc. While the immune system (lysoPAF) and secondary metabolite synthesis (aromatic amino acids and sulfhydryl compounds) facilitates fast growth and resistance to environmental stressors of P. meandrina, the cell membrane structure (structural lipids), energy storage (storage lipids), oxidative stress system (short peptides), and secondary metabolite synthesis (guanidine compounds) are beneficial to the survival of S. hystrix in harsh conditions. This study contributes to the understanding of the potential molecular traits underlying life-history strategies of different coral species.

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Ha, Van Thai, Duško Lainšček, Bernd Gesslbauer, Eva Jarc-Jovičić, Tuulia Hyötyläinen, Nejc Ilc, Katja Lakota et al. "Synergy between 15-lipoxygenase and secreted PLA2promotes inflammation by formation of TLR4 agonists from extracellular vesicles". Proceedings of the National Academy of Sciences 117, n.º 41 (24 de septiembre de 2020): 25679–89. http://dx.doi.org/10.1073/pnas.2005111117.

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Damage-associated endogenous molecules induce innate immune response, thus making sterile inflammation medically relevant. Stress-derived extracellular vesicles (stressEVs) released during oxidative stress conditions were previously found to activate Toll-like receptor 4 (TLR4), resulting in expression of a different pattern of immune response proteins in comparison to lipopolysaccharide (LPS), underlying the differences between pathogen-induced and sterile inflammation. Here we report that synergistic activities of 15-lipoxygenase (15-LO) and secreted phospholipase A2(sPLA2) are needed for the formation of TLR4 agonists, which were identified as lysophospholipids (lysoPLs) with oxidized unsaturated acyl chain. Hydroxy, hydroperoxy, and keto products of 2-arachidonoyl-lysoPI oxidation by 15-LO were identified by mass spectrometry (MS), and they activated the same gene pattern as stressEVs. Extracellular PLA2activity was detected in the synovial fluid from rheumatoid arthritis and gout patients. Furthermore, injection of sPLA2promoted K/BxN serum-induced arthritis in mice, whereby ankle swelling was partially TLR4 dependent. Results confirm the role of oxidized lysoPL of stressEVs in sterile inflammation that promotes chronic diseases. Both 15-LO and sPLA2enzymes are induced during inflammation, which opens the opportunity for therapy without compromising innate immunity against pathogens.

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Chau, L. Y., K. Peck, H. H. Yen y J. Y. Wang. "Agonist-induced down-regulation of platelet-activating factor receptor gene expression in U937 cells". Biochemical Journal 301, n.º 3 (1 de agosto de 1994): 911–16. http://dx.doi.org/10.1042/bj3010911.

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Prolonged exposure (8-24 h) of human promonocytic U937 cells to 100 nM 1-O-hexadecyl-2-N-methylcarbamyl-sn-glycero-3-phosphocholine (carbarmyl-PAF), a non-metabolizable analogue of platelet-activating factor (PAF), reduced the numbers of PAF receptors by 50-75%, as determined by the radioligand-binding assay. To clarify whether the down-regulation of receptor numbers is due to decreased expression level of the PAF-receptor gene, the effect of carbamyl-PAF on the steady-state level of PAF-receptor mRNA was examined by a highly sensitive reverse-transcriptase PCR method. A 50% decline in the level of PAF-receptor mRNA was observed in U937 cells pretreated with 100 nM carbamyl-PAF for 24 h. The effect of carbamyl-PAF was dose-dependent, with an EC50 value around 10 nM. PAF-receptor antagonist, SRI-63675, was able to attenuate the effect of carbamyl-PAF. Furthermore lysoPAF, at 1 uM, was unable to induce a significant decrease in PAF-receptor mRNA after incubation for 24 h, indicating that the effect of carbamyl-PAF was specific. The half-life of the PAF-receptor mRNA measured in the presence of actinomycin D was unaffected by carbamyl-PAF treatment. In contrast, nuclear run-off experiments demonstrated that the transcription rate of the PAF-receptor gene in carbamyl-PAF-treated cells was about 65% of that in control cells. These results suggest that the PAF receptor in U937 cells is subject to down-regulation by agonist, at least partly, at the transcriptional level.

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DiPersio, J., C. Abboud, S. Aggarwal y D. Golde. "72. GM-CSF directly induces neutrophil platelet activating factor (PAF) and leukotriene B4 (LTB4) synthesis: activation of the lysoPAF acetyltransferase through a tyrosine ki-nase-dependent signaling cascade". Biomedicine & Pharmacotherapy 46, n.º 5-7 (enero de 1992): 274. http://dx.doi.org/10.1016/0753-3322(92)90157-3.

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Aoyama, Chieko, Yasuhiro Horibata, Hiromi Ando, Satomi Mitsuhashi, Maki Arai y Hiroyuki Sugimoto. "Characterization of glycerophosphodiesterase 4-interacting molecules Gαq/11 and Gβ, which mediate cellular lysophospholipase D activity". Biochemical Journal 476, n.º 24 (17 de diciembre de 2019): 3721–36. http://dx.doi.org/10.1042/bcj20190666.

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We previously purified lysophospholipase D (lysoPLD), which hydrolyzes lysophosphatidylcholine (lysoPC) to lysophosphatidic acid (LPA), from rat brain and identified the heterotrimeric G protein subunits Gαq and Gβ1 in the lysoPLD active fractions. Tag-affinity purified Gαq exhibits lysoPLD activity but a mutant that affected cellular localization or interaction with the Gβ subunit reduced lysoPLD activity. Size exclusion chromatography revealed that active lysoPLD is a much higher molecular mass complex than is heterotrimeric G protein, suggesting the presence of other components. Liquid chromatography–tandem mass spectrometry of lysoPLD purified from rat brain identified glycerophosphodiesterase 4 (GDE4), recently reported as lysoPLD, in the same fraction as G proteins. The overexpressed and tag-purified Gαq fractions, which exhibit lysoPLD activity, contained GDE4. Exogenously expressed GDE4 was co-immunoprecipitated with endogenous Gαq and Gβ and exhibited high lysoPLD activity. The results of confocal microscopy and cell fractionation experiments indicated that exogenously expressed GDE4 in cells mainly localized at the endoplasmic reticulum and partially co-localized with Gαq protein at the plasma membrane. Proteinase K protection assay results suggested that the catalytic domain of GDE4 faces the lumen/extracellular space. Mutations at the conserved amino acids in the C-terminus cytoplasmic regions amongst GDE1, 4 and 7, dramatically suppressed GDE4 enzyme activities. When both the Gαq and Gα11 genes in Neuro2A cells were disrupted using the CRISPR–Cas9 system, endogenous lysoPLD activity was partially reduced but rescued by overexpression of Gαq. These results suggest that GDE4 is a new effector of G protein signaling that produces bioactive phospholipid LPA and/or modulates membrane homeostasis.

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Ou, Zhi-Jun, Li Li, Xiao-Long Liao, Yi-Ming Wang, Xiao-Xia Hu, Qing-Li Zhang, Zhi-Ping Wang et al. "Apolipoprotein A-I mimetic peptide inhibits atherosclerosis by altering plasma metabolites in hypercholesterolemia". American Journal of Physiology-Endocrinology and Metabolism 303, n.º 6 (15 de septiembre de 2012): E683—E694. http://dx.doi.org/10.1152/ajpendo.00136.2012.

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An apolipoprotein A-I mimetic peptide, D-4F, has been shown to improve vasodilation and inhibit atherosclerosis in hypercholesterolemic low-density lipoprotein receptor-null (LDLr−/−) mice. To study the metabolic variations of D-4F ininhibiting atherosclerosis, metabonomics, a novel system biological strategy to investigate the pathogenesis, was developed. Female LDLr−/− mice were fed a Western diet and injected with or without D-4F intraperitoneally. Atherosclerotic lesion formation was measured, whereas plasma metabolic profiling was obtained on the basis of ultra-high-performance liquid chromatography in tandem with time-of-flight mass spectrometry operating in both positive and negative ion modes. Data were processed by multivariate statistical analysis to graphically demonstrate metabolic changes. The partial least-squares discriminate analysis model was validated with cross-validation and permutation tests to ensure the model's reliability. D-4F significantly inhibited the formation of atherosclerosis in a time-dependent manner. The metabolic profiling was altered dramatically in hypercholesterolemic LDLr−/− mice, and a significant metabolic profiling change in response to D-4F treatment was observed in both positive and negative ion modes. Thirty-six significantly changed metabolites were identified as potential biomarkers. A series of phospholipid metabolites, including lysophosphatidylcholine (LysoPC), lysophosphatidylethanolamine (LysoPE), phosphatidylcholine (PC), phatidylethanolamine (PE), sphingomyelin (SM), and diacylglycerol (DG), particularly the long-chain LysoPC, was elevated dramatically in hypercholesterolemic LDLr−/− mice but reduced by D-4F in a time-dependent manner. Quantitative analysis of LysoPC, LysoPE, PC, and DG using HPLC was chosen to validate the variation of these potential biomarkers, and the results were consistent with the metabonomics findings. Our findings demonstrated that D-4F may inhibit atherosclerosis by regulating phospholipid metabolites specifically by decreasing plasma long-chain LysoPC.

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Schleimer, R. P., D. A. Davidson, L. M. Lichtenstein y N. F. Adkinson. "Selective inhibition of arachidonic acid metabolite release from human lung tissue by antiinflammatory steroids." Journal of Immunology 136, n.º 8 (15 de abril de 1986): 3006–11. http://dx.doi.org/10.4049/jimmunol.136.8.3006.

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Abstract The effects of antiinflammatory steroids on arachidonic acid metabolite release from human lung fragments were analyzed. Incubation of lung fragments for 24 hr with 10(-6) M dexamethasone inhibited the net release of the prostacyclin metabolite 6-keto-PGF1 alpha, PGE2, and PGF2 alpha from lung fragments stimulated with anti-IgE but failed to inhibit the anti-IgE-induced release of PGD2, TXB2, and iLTC4. The IC50 of dexamethasone for inhibition of both spontaneous and anti-IgE-induced 6-keto-PGF1 alpha release was approximately 2 X 10(-8) M, and a 6-hr preincubation with the drug was required for 50% inhibition of prostaglandin release. Other agents were tested for activity in stimulating arachidonic acid metabolite release from human lung fragments. FMLP (fmet-leu-phe) stimulated the release of all metabolites tested (6-keto-PGF1 alpha, PGD2, PGE2, PGF2 alpha, TXB2, iLTC4); platelet-activating factor (PAF), but not lysoPAF, stimulated the release of PGD2, TXB2, and iLTC4. In contrast to the case with anti-IgE, where dexamethasone failed to inhibit net PGD2 and TXB2 release, the steroid inhibited the release of these metabolites stimulated by both FMLP and PAF. The steroid inhibited iLTC4 release induced by the highest concentration of PAF (10(-6)M) but did not inhibit iLTC4 release stimulated by either 10(-7) M PAF, FMLP, or anti-IgE. Because neither FMLP nor PAF caused the release of PGD2 or TXB2 from purified human lung mast cells, and because they also failed to induce histamine release from lung fragments, it is suggested that these stimuli produce PGD2 and TXB2 release in lung fragments through an action on a cell distinct from the mast cell. This suggestion is supported by the selective inhibition of the release of these arachidonic acid metabolites by dexamethasone. We suggest that the inhibitory action of steroids on arachidonic acid metabolite in human lung fragments contributes to their therapeutic efficacy in pulmonary diseases.

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Kim, Yeon-Hee, Jin-Soo Chung, Hyung-Ho Lee, Jin-Hee Park y Mi-Kyung Kim. "Influence of Dietary Polyunsaturated Fatty Acid Intake on Potential Lipid Metabolite Diagnostic Markers in Renal Cell Carcinoma: A Case-Control Study". Nutrients 16, n.º 9 (24 de abril de 2024): 1265. http://dx.doi.org/10.3390/nu16091265.

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Non-invasive diagnostics are crucial for the timely detection of renal cell carcinoma (RCC), significantly improving survival rates. Despite advancements, specific lipid markers for RCC remain unidentified. We aimed to discover and validate potent plasma markers and their association with dietary fats. Using lipid metabolite quantification, machine-learning algorithms, and marker validation, we identified RCC diagnostic markers in studies involving 60 RCC and 167 healthy controls (HC), as well as 27 RCC and 74 HC, by analyzing their correlation with dietary fats. RCC was associated with altered metabolism in amino acids, glycerophospholipids, and glutathione. We validated seven markers (l-tryptophan, various lysophosphatidylcholines [LysoPCs], decanoylcarnitine, and l-glutamic acid), achieving a 96.9% AUC, effectively distinguishing RCC from HC. Decreased decanoylcarnitine, due to reduced carnitine palmitoyltransferase 1 (CPT1) activity, was identified as affecting RCC risk. High intake of polyunsaturated fatty acids (PUFAs) was negatively correlated with LysoPC (18:1) and LysoPC (18:2), influencing RCC risk. We validated seven potential markers for RCC diagnosis, highlighting the influence of high PUFA intake on LysoPC levels and its impact on RCC occurrence via CPT1 downregulation. These insights support the efficient and accurate diagnosis of RCC, thereby facilitating risk mitigation and improving patient outcomes.

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Cao, C., H. Shi, M. Zhang, L. Bo, L. Hu, S. Li, S. Chen et al. "Metabonomic analysis of toxic action of long-term low-level exposure to acrylamide in rat serum". Human & Experimental Toxicology 37, n.º 12 (16 de abril de 2018): 1282–92. http://dx.doi.org/10.1177/0960327118769708.

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This study assessed the effects of long-term, low-dose acrylamide (AA) administration in rats using ultra-performance liquid chromatography–mass spectrometry. Forty male Wistar rats were randomly divided into the following four groups: control, low-dose AA (0.2 mg/kg BW), middle-dose AA (1 mg/kg BW), and high-dose AA (5 mg/kg BW). AA was administered to rats via drinking water ad libitum. After 16-week treatment, rat serum was collected for metabonomic analysis. Biochemical tests were further conducted to verify metabolic alterations. Eleven metabolites were identified with significant changes in intensities (increased or reduced) as a result of treatment. These metabolites included citric acid, pantothenic acid, isobutyryl-l-carnitine, eicosapentaenoic acid, docosahexaenoic acid, sphingosine 1-phosphate, LysoPC(20:4), LysoPC(22:6), LysoPE(20:3), undecanedioic acid, and dodecanedioic acid. Results indicate that chronic exposure to AA at no observed adverse effect level does not exert a toxic effect on rats at the body metabolism level. AA disturbed the metabolism of lipids and energy, affected the nervous system of rats, and induced oxidative stress and liver dysfunction.

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Hofmanová, Jiřina, Josef Slavík, Miroslav Ciganek, Petra Ovesná, Zuzana Tylichová, Martina Karasová, Ondřej Zapletal et al. "Complex Alterations of Fatty Acid Metabolism and Phospholipidome Uncovered in Isolated Colon Cancer Epithelial Cells". International Journal of Molecular Sciences 22, n.º 13 (22 de junio de 2021): 6650. http://dx.doi.org/10.3390/ijms22136650.

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The development of colon cancer, one of the most common malignancies, is accompanied with numerous lipid alterations. However, analyses of whole tumor samples may not always provide an accurate description of specific changes occurring directly in tumor epithelial cells. Here, we analyzed in detail the phospholipid (PL), lysophospholipid (lysoPL), and fatty acid (FA) profiles of purified EpCAM+ cells, isolated from tumor and adjacent non-tumor tissues of colon cancer patients. We found that a number of FAs increased significantly in isolated tumor cells, which also included a number of long polyunsaturated FAs. Higher levels of FAs were associated with increased expression of FA synthesis genes, as well as with altered expression of enzymes involved in FA elongation and desaturation, including particularly fatty acid synthase, stearoyl-CoA desaturase, fatty acid desaturase 2 and ELOVL5 fatty acid elongase 5 We identified significant changes in ratios of specific lysoPLs and corresponding PLs. A number of lysophosphatidylcholine and lysophosphatidylethanolamine species, containing long-chain and very-long chain FAs, often with high numbers of double bonds, were significantly upregulated in tumor cells. Increased de novo synthesis of very long-chain FAs, or, altered uptake or incorporation of these FAs into specific lysoPLs in tumor cells, may thus contribute to reprogramming of cellular phospholipidome and membrane alterations observed in colon cancer.

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MODHA, J., M. C. ROBERTS, W. M. ROBERTSON, G. SWEETMAN, K. A. POWELL, M. W. KENNEDY y J. R. KUSEL. "The surface coat of infective larvae of Trichinella spiralis". Parasitology 118, n.º 5 (mayo de 1999): 509–22. http://dx.doi.org/10.1017/s0031182099004266.

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The surface coat of the infective larvae of the parasitic nematode Trichinella spiralis was characterized with respect to its biophysical properties, morphology and composition. Labelling of larvae with the fluorescent surface probe PKH26 was lost after activation (by incubation in mammalian medium containing trypsin and bile), or following pronase treatment. Electron microscopical examination revealed that pronase treatment resulted in the loss of an amorphous surface layer only, further demonstrating the specificity of PKH26 for the larval surface coat. Surface coat shedding was inhibited by sodium azide and carbonyl cyanide, or by incubation of larvae at 4°C, suggesting the shedding process required metabolic energy. Pre-labelled, unactivated larvae demonstrated continuous slow surface coat shedding and could be re-labelled with PKH26, indicating that the shed coat is replaced in these parasites. However, pre-labelled larvae which were activated failed to re-label with the probe, suggesting that activation provides an irreversible trigger for surface changes. PKH26, therefore, is a useful marker for larval activation. Examination of the shed coat material by scanning electron microscopy revealed 2 types of morphologies; one comprising thin multilaminate sheets and the other of amorphous material with ridges producing a fingerprint-like motif. Western- and lectin-blotting of the shed coat material demonstrated 2 prominent entities; a 90 kDa glycoprotein, which bound Datura stramonium agglutinin and was resistant to N- and O-glycanase treatment and a 47–60 kDa set of protein(s). Analysis of the surface lipids by electrospray mass spectometry revealed the presence of lysophosphatidic acid (lysoPA, C14[ratio ]2) and an unidentifiable component of 339·4 Da. These two lipids constituted 36·9% and 36% by mass of surface coat lipids respectively. The presence of lysoPA was confirmed by thin layer chromatography, which also detected phosphatidic acid (PA). The polar lipids detected in solvent rinses of intact parasites by electrospray mass spectrometry were PI (C48[ratio ]4), PE (C40[ratio ]4 and C38[ratio ]4), PS (C40[ratio ]4), lysoPC (C20[ratio ]2 and C18[ratio ]2) and lysoPA (C14[ratio ]2). These observations are discussed with respect to the role of the surface coat and its shedding in the T. spiralis host–parasite relationship.

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Wu, Hongyu, Mikhail Bogdanov, Yujin Zhang, Kaiqi Sun, Anren Song, Hong Liu, Morayo G, Adebiyi et al. "Metabolomic Profiling Identifies Hypoxia-Induced Imbalanced Lands' Cycle Promotes Sickling and Disease Progression". Blood 126, n.º 23 (3 de diciembre de 2015): 2134. http://dx.doi.org/10.1182/blood.v126.23.2134.2134.

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Abstract Sickle cell disease (SCD) is a prevalent hemolytic genetic disorder with high morbidity and mortality affecting millions of individuals worldwide. Although it is well accepted that deoxygenation and polymerization of sickle hemoglobin (HbS) are initial triggers for sickling, it has been known for more than three decades that abnormal membrane lipid organization and composition are found in sickle erythrocyte. Early studies showed some lipids are altered in sickle erythrocytes, however, no studies have identified overall membrane lipid alteration and functional role of those altered specific lipids in SCD. Using unbiased metabolomic profiling, we found that lysophospholipids (LPLs), particularly lysophosphocholines (LysoPCs), were significantly elevated inside erythrocytes of mice with SCD due to imbalanced Lands' cycle. Lands' cycle containing two concerted enzymes: phospholipases A2 (PLA2s) and lysophospholipid acyltransferases (LPLATs) was initially discovered in 1958. However, its function and cellular regulation in membrane homeostasis in SCD remain unrecognized prior to our metabolomics screening. Here, we demonstrated that enhancing imbalanced Lands' cycle promotes a process of sickling and disease progression in mice by inducing LysoPC content inside erythrocytes. Significantly, correcting impaired Lands' cycle reduced LysoPC levels within erythrocytes and attenuated sickling and disease progression in mice. Mechanistically, we revealed that hypoxia-mediated MEK/ERK activation underlies imbalanced Lands' cycle by preferentially inducing activity of PLA2 but not LPCAT1 in mouse sickle erythrocytes. Additionally, the detrimental role of impaired Lands' cycle-induced LysoPC production in sickling via MEK/ERK-dependent activation of PLA2 in SCD patients mirrors our mouse finding. Overall, our studies have identified a pathological role of imbalanced Lands' cycle in SCD, revealed molecular basis regulating Lands' cycle and immediately provided novel therapeutic possibilities for the disease. Disclosures No relevant conflicts of interest to declare.

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Kim, Min Jung, Hye Jeong Yang, Jin Hee Kim, Chang-Won Ahn, Jong Ho Lee, Kang Sung Kim y Dae Young Kwon. "Obesity-Related Metabolomic Analysis of Human Subjects in Black Soybean Peptide Intervention Study by Ultraperformance Liquid Chromatography and Quadrupole-Time-of-Flight Mass Spectrometry". Journal of Obesity 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/874981.

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The present study aimed to identify key metabolites related to weight reduction in humans by studying the metabolic profiles of sera obtained from 34 participants who underwent dietary intervention with black soybean peptides (BSP) for 12 weeks. This research is a sequel to our previous work in which the effects of BSP on BMI and blood composition of lipid were investigated. Sera of the study were subjected to ultra performance liquid chromatography and quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS), and the data were analyzed using partial least-squares discriminate analysis (PLS-DA) score plots. Body mass index and percent body fat of the test group were reduced. Levels of betaine, benzoic acid, pyroglutamic acid, pipecolic acid,N-phenylacetamide, uric acid,l-aspartyl-l-phenylalanine, and lysophosphatidyl cholines (lysoPCs) (C18:1, C18:2, C20:1, and C20:4) showed significant increases. Levels ofl-proline, valine,l-leucine/isoleucine, hypoxanthine, glutamine,l-methionine, phenylpyruvic acid, several carnitine derivatives, and lysoPCs (C14:0, PC16:0, C15:0, C16:0, C17:1, C18:0, and C22:0) were significantly decreased. In particular, lysoPC 16:0 with a VIP value of 12.02 is esteemed to be the most important metabolite for evaluating the differences between the 2 serum samples. Our result confirmed weight-lowering effects of BSP, accompanied by favorable changes in metabolites in the subjects’ blood. Therefore, this research enables us to better understand obesity and increases the predictability of the obesity-related risk by studying metabolites present in the blood.

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Nenu, Iuliana, Horia Stefanescu, Bogdan Procopet, Zeno Sparchez, Iulia Minciuna, Tudor Mocan, Daniel Leucuta et al. "Navigating through the Lipid Metabolism Maze: Diagnosis and Prognosis Metabolites of Hepatocellular Carcinoma versus Compensated Cirrhosis". Journal of Clinical Medicine 11, n.º 5 (26 de febrero de 2022): 1292. http://dx.doi.org/10.3390/jcm11051292.

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(1) Background: The pursuit of finding biomarkers for the diagnosis and prognosis of hepatocellular carcinoma (HCC) has never been so paramount in the days of personalized medicine. The main objective of our study is to identify new biomarkers for diagnosing HCC, and to identify which patients are at risk of developing tumor recurrence, decompensation, or even possesses the risk of cancer-related death. (2) Methods: We have conducted an untargeted metabolomics study from the serum of 69 European patients—32 compensated cirrhotic patients without HCC (controls), and 37 cirrhotic patients with HCC with compensated underlying liver disease (cases), that underwent curative treatment (surgery or ablation), performing ultra-high-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight mass spectrometry (UHPLC-QTOF- (ESI+)-MS) with an emphasis on lipid metabolites. (3) Results: 1,25-dihydroxy cholesterol (m/z = 419.281), myristyl palmitate (m/z = 453.165), 25-hydroxy vitamin D2 (m/z = 413.265), 12-ketodeoxycholic acid (m/z = 391.283), lysoPC (21:4) (m/z = 558.291), and lysoPE (22:2) (m/z = 534.286) represent notable biomarkers that differentiate compensated cirrhosis from early HCC, and ceramide species are depleted in the serum of HCC patients. Regarding prognosis, no metabolite identified in our study could determine tumor relapse. To distinguish between the HCC patients that survived curative treatment and those at risk that developed tumor burden, we have identified two notable phosphocholines (PC (30:2); PC (30:1)) with AUROCs of 0.820 and 0.807, respectively, that seem to increase when patients are at risk. In a univariate analysis, arachidonic acid was the only metabolite to predict decompensation (OR = 0.1, 95% CI: 0–0.16, p < 0.005), while in the multivariate analysis, dismally, no variable was associated with decompensation. Furthermore, in the multivariate analysis, we have found out for the first time that the increased expression of 1,25-dihydroxy cholesterol, myristyl palmitate, 12-keto deoxycholic acid, lysoPC (21:4), and lysoPE (22:2) are independent markers of survival. (4) Conclusions: Our study reveals that lipids play a crucial role in discriminating compensated cirrhosis and early hepatocellular carcinoma, and might represent markers of survival and prognosis in personalized and minimally invasive medicine.

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Key, Chia-Chi C., Andrew C. Bishop, Xianfeng Wang, Qingxia Zhao, Guan-yuan Chen, Matthew A. Quinn, Xuewei Zhu, Qibin Zhang y John S. Parks. "Human GDPD3 overexpression promotes liver steatosis by increasing lysophosphatidic acid production and fatty acid uptake". Journal of Lipid Research 61, n.º 7 (19 de mayo de 2020): 1075–86. http://dx.doi.org/10.1194/jlr.ra120000760.

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The glycerol phosphate pathway produces more than 90% of the liver triacylglycerol (TAG). LysoPA, an intermediate in this pathway, is produced by glycerol-3-phosphate acyltransferase. Glycerophosphodiester phosphodiesterase domain containing 3 (GDPD3), whose gene was recently cloned, contains lysophospholipase D activity, which produces LysoPA from lysophospholipids. Whether human GDPD3 plays a role in hepatic TAG homeostasis is unknown. We hypothesized that human GDPD3 increases LysoPA production and availability in the glycerol phosphate pathway, promoting TAG biosynthesis. To test our hypothesis, we infected C57BL/6J mice with adeno-associated virus encoding a hepatocyte-specific albumin promoter that drives GFP (control) or FLAG-tagged human GDPD3 overexpression and fed the mice chow or a Western diet to induce hepatosteatosis. Hepatic human GDPD3 overexpression induced LysoPA production and increased FA uptake and incorporation into TAG in mouse hepatocytes and livers, ultimately exacerbating Western diet-induced liver steatosis. Our results also showed that individuals with hepatic steatosis have increased GDPD3 mRNA levels compared with individuals without steatosis. Collectively, these findings indicate that upregulation of GDPD3 expression may play a key role in hepatic TAG accumulation and may represent a molecular target for managing hepatic steatosis.

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Xie, Ting, Chuxiang Lei, Wei Song, Xunyao Wu, Jianqiang Wu, Fangyuan Li, Yanze Lv, Yuexin Chen, Bao Liu y Yuehong Zheng. "Plasma Lipidomics Analysis Reveals the Potential Role of Lysophosphatidylcholines in Abdominal Aortic Aneurysm Progression and Formation". International Journal of Molecular Sciences 24, n.º 12 (16 de junio de 2023): 10253. http://dx.doi.org/10.3390/ijms241210253.

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Abdominal aortic aneurysm (AAA) is hallmarked by irreversible dilation of the infrarenal aorta. Lipid deposition in the aortic wall and the potential importance of a lipid disorder in AAA etiology highlight the need to explore lipid variation during AAA development. This study aimed to systematically characterize the lipidomics associated with AAA size and progression. Plasma lipids from 106 subjects (36 non-AAA controls and 70 AAA patients) were comprehensively analyzed using untargeted lipidomics. An AAA animal model was established by embedding angiotensin-II pump in ApoE-/- mice for four weeks and blood was collected at 0, 2 and 4 weeks for lipidomic analysis. Using a false-discovery rate (FDR) < 0.05, a group of lysophosphatidylcholines (lysoPCs) were specifically decreased in AAA patients and mice. LysoPCs were principally lower in the AAA patients with larger diameter (diameter > 50 mm) than those with a smaller size (30 mm < diameter < 50 mm), and levels of lysoPCs were also found to be decreased with modelling time and aneurysm formation in AAA mice. Correlation matrices between lipids and clinical characteristics identified that the positive correlation between lysoPCs and HDL-c was reduced and negative correlations between lysoPCs and CAD rate, lysoPCs and hsCRP were converted to positive correlations in AAA compared to control. Weakened positive correlations between plasma lysoPCs and circulating HDL-c in AAA suggested that HDL-lysoPCs may elicit instinctive physiological effects in AAA. This study provides evidence that reduced lysoPCs essentially underlie the pathogenesis of AAA and that lysoPCs are promising biomarkers for AAA development.

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Cheng, Mei-Ling, Hsiang-Yu Tang, Pei-Ting Wu, Cheng-Hung Yang, Chi-Jen Lo, Jui-Fen Lin y Hung-Yao Ho. "7-Ketocholesterol Induces Lipid Metabolic Reprogramming and Enhances Cholesterol Ester Accumulation in Cardiac Cells". Cells 10, n.º 12 (20 de diciembre de 2021): 3597. http://dx.doi.org/10.3390/cells10123597.

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7-Ketocholesterol (7KCh) is a major oxidized cholesterol product abundant in lipoprotein deposits and atherosclerotic plaques. Our previous study has shown that 7KCh accumulates in erythrocytes of heart failure patients, and further investigation centered on how 7KCh may affect metabolism in cardiomyocytes. We applied metabolomics to study the metabolic changes in cardiac cell line HL-1 after treatment with 7KCh. Mevalonic acid (MVA) pathway-derived metabolites, such as farnesyl-pyrophosphate and geranylgeranyl-pyrophosphate, phospholipids, and triacylglycerols levels significantly declined, while the levels of lysophospholipids, such as lysophosphatidylcholines (lysoPCs) and lysophosphatidylethanolamines (lysoPEs), considerably increased in 7KCh-treated cells. Furthermore, the cholesterol content showed no significant change, but the production of cholesteryl esters was enhanced in the treated cells. To explore the possible mechanisms, we applied mRNA-sequencing (mRNA-seq) to study genes differentially expressed in 7KCh-treated cells. The transcriptomic analysis revealed that genes involved in lipid metabolic processes, including MVA biosynthesis and cholesterol transport and esterification, were differentially expressed in treated cells. Integrated analysis of both metabolomic and transcriptomic data suggests that 7KCh induces cholesteryl ester accumulation and reprogramming of lipid metabolism through altered transcription of such genes as sterol O-acyltransferase- and phospholipase A2-encoding genes. The 7KCh-induced reprogramming of lipid metabolism in cardiac cells may be implicated in the pathogenesis of cardiovascular diseases.

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Goldberg, Erin, Shiva Ievari-Shariati, Biniam Kidane, Julian Kim, Shantanu Banerji, Gefei Qing, Sadeesh Srinathan, Leigh Murphy y Michel Aliani. "Comparative metabolomics studies of blood collected in streck and heparin tubes from lung cancer patients". PLOS ONE 16, n.º 4 (23 de abril de 2021): e0249648. http://dx.doi.org/10.1371/journal.pone.0249648.

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Metabolomics analysis of blood from patients (n = 42) undergoing surgery for suspected lung cancer was performed in this study. Venous and arterial blood was collected in both Streck and Heparin tubes. A total of 96 metabolites were detected, affected by sex (n = 56), collection tube (n = 33), and blood location (n = 8). These metabolites belonged to a wide array of compound classes including lipids, acids, pharmaceutical agents, signalling molecules, vitamins, among others. Phospholipids and carboxylic acids accounted for 28% of all detected compounds. Out of the 33 compounds significantly affected by collection tube, 18 compounds were higher in the Streck tubes, including allantoin and ketoleucine, and 15 were higher in the Heparin tubes, including LysoPC(P-16:0), PS 40:6, and chenodeoxycholic acid glycine conjugate. Based on our results, it is recommended that replicate blood samples from each patient should be collected in different types of blood collection tubes for a broader range of the metabolome. Several metabolites were found at higher concentrations in cancer patients such as lactic acid in Squamous Cell Carcinoma, and lysoPCs in Adenocarcinoma and Acinar Cell Carcinoma, which may be used to detect early onset and/or to monitor the progress of the cancer patients.

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Stoll, L. L., H. J. Oskarsson y A. A. Spector. "Interaction of lysophosphatidylcholine with aortic endothelial cells". American Journal of Physiology-Heart and Circulatory Physiology 262, n.º 6 (1 de junio de 1992): H1853—H1860. http://dx.doi.org/10.1152/ajpheart.1992.262.6.h1853.

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To better understand the vascular actions of lysophosphatidylcholine (lysoPC), we studied the interaction of [1-14C]palmitate-labeled lysoPC with bovine aortic endothelial cells. These cells took up lysoPC from media containing albumin, low-density lipoproteins (LDL), or acetyl-LDL. Uptake occurred faster than conversion to phosphatidylcholine (PC), leading to some lysoPC accumulation in endothelial lipids. Endothelial cell monolayers grown on micropore filters took up lysoPC from both apical and basolateral surfaces, preventing substantial amounts from passage across the endothelial monolayer. However, lysoPC present in the interstitial medium of an endothelial-smooth muscle coculture was incorporated primarily by the smooth muscle cells. Endothelial cells grown on filters released lysoPC into both the apical and basolateral medium in the presence of albumin or lipoproteins. Exposure to 50 microM lysoPC produced no evidence of endothelial cytotoxicity, but prostaglandin (PG)I2 production was reduced. These studies suggest that the endothelium can participate in the processing of circulating lysoPC and, through basolateral uptake, can facilitate the removal of lysoPC formed within the arterial wall. By decreasing PGI2 output, however, exposure to high concentrations of lysoPC may reduce the antithrombotic and vasodilator capacity of the endothelium.

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Li, Jun, Xiaojun Liao, Xuedong Yin, Zimeng Deng, Guangfen Hu, Weiwei Zhang, Feng Jiang y Liang Zhao. "Gut Microbiome and Serum Metabolome Profiles of Capsaicin with Cognitive Benefits in APP/PS1 Mice". Nutrients 15, n.º 1 (27 de diciembre de 2022): 118. http://dx.doi.org/10.3390/nu15010118.

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Capsaicin, a natural bioactive component, has been reported to improve cognition and ameliorate the pathology of Alzheimer’s disease (AD). Studies have linked AD to alterations in gut microbiota composition and serum metabolites. In the present study, we examined the alterations in serum metabolome and gut microbiome in APPswe/PS1dE9 (APP/PS1) mice treated with capsaicin. Capsaicin treatments resulted in a significant increase in the abundance of Akkermansia, Faecalibaculum, Unclassified_f_Atopobiaceae, and Gordonibacter and a significant decrease in the abundance of Adlercreutzia, Peptococcaceae, Alistipes, Oscillibacter and Erysipelatoclostridium. Furthermore, the species Akkermansia muciniphila (A. muciniphila) was significantly enriched in capsaicin-treated APP/PS1 mice (p = 0.0002). Serum metabolomic analysis showed that capsaicin-treated APP/PS1 mice had a significant higher level of tryptophan (Trp) metabolism and a significantly lower level of lipid metabolism compared with vehicle-treated mice. Capsaicin altered serum metabolites, including Kynurenine (Kyn), 5-Hydroxy-L-tryptophan (5-HIT), 5-Hydroxyindoleacetic acid (5-HIAA), indoxylsulfuric acid, lysophosphatidyl cholines (LysoPCs), and lysophosphatidyl ethanolamine (LysoPE). Significant correlations were observed between the gut bacteria and serum metabolite. With regard to the increased abundance of A. muciniphila and the ensuing rise in tryptophan metabolites, our data show that capsaicin alters both the gut microbiota and blood metabolites. By altering the gut microbiome and serum metabolome, a diet high in capsaicin may reduce the incidence and development of AD.

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Jong, Cholnam, Zhenhai Yu, Yu Zhang, Kyongho Choe, Songrok Uh, Kibong Kim, Chol Jong et al. "Multi-Omics Analysis of a Chromosome Segment Substitution Line Reveals a New Regulation Network for Soybean Seed Storage Profile". International Journal of Molecular Sciences 25, n.º 11 (21 de mayo de 2024): 5614. http://dx.doi.org/10.3390/ijms25115614.

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Soybean, a major source of oil and protein, has seen an annual increase in consumption when used in soybean-derived products and the broadening of its cultivation range. The demand for soybean necessitates a better understanding of the regulatory networks driving storage protein accumulation and oil biosynthesis to broaden its positive impact on human health. In this study, we selected a chromosome segment substitution line (CSSL) with high protein and low oil contents to investigate the underlying effect of donor introgression on seed storage through multi-omics analysis. In total, 1479 differentially expressed genes (DEGs), 82 differentially expressed proteins (DEPs), and 34 differentially expressed metabolites (DEMs) were identified in the CSSL compared to the recurrent parent. Based on Gene Ontology (GO) term analysis and the Kyoto Encyclopedia of Genes and Genomes enrichment (KEGG), integrated analysis indicated that 31 DEGs, 24 DEPs, and 13 DEMs were related to seed storage functionality. Integrated analysis further showed a significant decrease in the contents of the seed storage lipids LysoPG 16:0 and LysoPC 18:4 as well as an increase in the contents of organic acids such as L-malic acid. Taken together, these results offer new insights into the molecular mechanisms of seed storage and provide guidance for the molecular breeding of new favorable soybean varieties.

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Sim, Myeong Seong, Hye Jeong Kim, Sang Hee Jo, Chun Kim y Il Yup Chung. "Lysophosphatidylserine Induces MUC5AC Production via the Feedforward Regulation of the TACE-EGFR-ERK Pathway in Airway Epithelial Cells in a Receptor-Independent Manner". International Journal of Molecular Sciences 23, n.º 7 (31 de marzo de 2022): 3866. http://dx.doi.org/10.3390/ijms23073866.

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Lysophosphatidylserine (LysoPS) is an amphipathic lysophospholipid that mediates a broad spectrum of inflammatory responses through a poorly characterized mechanism. Because LysoPS levels can rise in a variety of pathological conditions, we sought to investigate LysoPS’s potential role in airway epithelial cells that actively participate in lung homeostasis. Here, we report a previously unappreciated function of LysoPS in production of a mucin component, MUC5AC, in the airway epithelial cells. LysoPS stimulated lung epithelial cells to produce MUC5AC via signaling pathways involving TACE, EGFR, and ERK. Specifically, LysoPS- dependent biphasic activation of ERK resulted in TGF-α secretion and strong EGFR phosphorylation leading to MUC5AC production. Collectively, LysoPS induces the expression of MUC5AC via a feedback loop composed of proligand synthesis and its proteolysis by TACE and following autocrine EGFR activation. To our surprise, we were not able to find a role of GPCRs and TLR2, known LyoPS receptors in LysoPS-induced MUC5AC production in airway epithelial cells, suggesting a potential receptor-independent action of LysoPS during inflammation. This study provides new insight into the potential function and mechanism of LysoPS as an emerging lipid mediator in airway inflammation.

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Yamamoto, Yusuke, Toshihiro Sakurai, Zhen Chen, Nao Inoue, Hitoshi Chiba y Shu-Ping Hui. "Lysophosphatidylethanolamine Affects Lipid Accumulation and Metabolism in a Human Liver-Derived Cell Line". Nutrients 14, n.º 3 (28 de enero de 2022): 579. http://dx.doi.org/10.3390/nu14030579.

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The physiological functions of lysophosphatidylethanolamine (lysoPE) have not been fully elucidated. In this study, the effects of lysoPE on lipogenesis and lipolysis were investigated in a cultured human liver-derived cell line. The intracellular lipid profile was investigated in detail using liquid chromatography–tandem mass spectrometry (LC-MS/MS) to better understand the underlying mechanism. The expression of genes related to lipid metabolism and catabolism was analyzed using real-time PCR. LysoPE supplementation induced cellular lipid droplet formation and altered triacylglycerol (TAG) profiles. Furthermore, lysoPE downregulated expression of the TAG hydrolyzation regulation factor ATGL, and reduced the expression of fatty acid biosynthesis-related genes SREBP1 and SCD1. LC-MS/MS-based lipidomic profiling revealed that the addition of lysoPE 18:2 increased the PE species containing linoleic acyl, as well as the CE 18:2 species, likely due to the incorporation of linoleic acyl from lysoPE 18:2. Collectively, these findings suggest that lysoPE 18:2 is involved in lipid droplet formation by suppressing lipolysis and fatty acid biosynthesis. Thus, lysoPE might play a pathological role in the induction of fatty liver disease.

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Sawada, Naoko, Takashi Obama, Mirei Mizuno, Kiyoshi Fukuhara, Sanju Iwamoto, Toshihiro Aiuchi, Tomohiko Makiyama y Hiroyuki Itabe. "Transfer and Enzyme-Mediated Metabolism of Oxidized Phosphatidylcholine and Lysophosphatidylcholine between Low- and High-Density Lipoproteins". Antioxidants 9, n.º 11 (26 de octubre de 2020): 1045. http://dx.doi.org/10.3390/antiox9111045.

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Oxidized low-density lipoprotein (oxLDL) and oxidized high-density lipoprotein (oxHDL), known as risk factors for cardiovascular disease, have been observed in plasma and atheromatous plaques. In a previous study, the content of oxidized phosphatidylcholine (oxPC) and lysophosphatidylcholine (lysoPC) species stayed constant in isolated in vivo oxLDL but increased in copper-induced oxLDL in vitro. In this study, we prepared synthetic deuterium-labeled 1-palmitoyl lysoPC and palmitoyl-glutaroyl PC (PGPC), a short chain-oxPC to elucidate the metabolic fate of oxPC and lysoPC in oxLDL in the presence of HDL. When LDL preloaded with d13-lysoPC was mixed with HDL, d13-lysoPC was recovered in both the LDL and HDL fractions equally. d13-LysoPC decreased by 50% after 4 h of incubation, while d13-PC increased in both fractions. Diacyl-PC production was abolished by an inhibitor of lecithin-cholesterol acyltransferase (LCAT). When d13-PGPC-preloaded LDL was incubated with HDL, d13-PGPC was transferred to HDL in a dose-dependent manner when both LCAT and lipoprotein-associated phospholipase A2 (Lp-PLA2) were inhibited. Lp-PLA2 in both HDL and LDL was responsible for the hydrolysis of d13-PGPC. These results suggest that short chain-oxPC and lysoPC can transfer between lipoproteins quickly and can be enzymatically converted from oxPC to lysoPC and from lysoPC to diacyl-PC in the presence of HDL.

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Niewoehner, D. E., K. Rice, A. A. Sinha y D. Wangensteen. "Injurious effects of lysophosphatidylcholine on barrier properties of alveolar epithelium". Journal of Applied Physiology 63, n.º 5 (1 de noviembre de 1987): 1979–86. http://dx.doi.org/10.1152/jappl.1987.63.5.1979.

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We studied the effects of lysophosphatidylcholine (lysoPC) on the barrier properties and the morphology of the alveolar-capillary membrane in isolated, fluid-filled hamster lungs continuously perfused. When instilled into the airspace at initial concentrations of 8–128 micrograms/ml, lysoPC causes dose-dependent increases in the permeability-surface area product of the alveolar epithelium for small (14C-sucrose, 342) and large (125I-neutral dextran, 70,000) solutes, with maximal values for each solute approximately 15 times control. Rapid whole-lung weight gains are caused by 128 micrograms lysoPC per milliliter, but each of the lower concentrations has no effect on net lung water balance. Electron-microscopic studies demonstrate that type I pneumonocytes are the lung cells most susceptible to lysoPC exposure, with cell swelling being the most prominent feature from low-dose exposure with more severe disruptive changes at the highest concentration tested. The effects of lysoPC are relatively specific, as several structurally related lipids have little or no effect at equivalent concentrations. Instillation of phospholipase A2 causes functional changes similar to those seen with lysoPC, presumably by generation of lysoPC from endogenous phospholipids. Studies employing a 14C-radiolabeled compound show that instilled lysoPC rapidly partitions into the lung lipid fraction where a major portion of the acyl group becomes incorporated into phosphatidylcholine. The amount of instilled lysoPC required to produce functional and morphological effects comprises only a few percent of total lung phospholipids. Since lysoPC is a normal component of lung phospholipids, severe lung dysfunction might result from minor abnormalities in the formation or degradation of this compound.

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Hervé, Perrine, Sarah Monic, Frédéric Bringaud y Loïc Rivière. "Phospholipases A and Lysophospholipases in protozoan parasites". Microbial Cell 10, n.º 10 (2 de octubre de 2023): 204–16. http://dx.doi.org/10.15698/mic2023.10.805.

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Phospholipases (PLs) and Lysophospholipases (LysoPLs) are a diverse group of esterases responsible for phospholipid or lysophospholipid hydrolysis. They are involved in several biological processes, including lipid catabolism, modulation of the immune response and membrane maintenance. PLs are classified depending on their site of hydrolysis as PLA1, PLA2, PLC and PLD. In many pathogenic microorganisms, from bacteria to fungi, PLAs and LysoPLs have been described as critical virulence and/or pathogenicity factors. In protozoan parasites, a group containing major human and animal pathogens, growing literature show that PLAs and LysoPLs are also involved in the host infection. Their ubiquitous presence and role in host-pathogen interactions make them particularly interesting to study. In this review, we summarize the literature on PLAs and LysoPLs in several protozoan parasites of medical relevance, and discuss the growing interest for them as potential drug and vaccine targets.

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Gao, Ya-Nan, Chen-Qing Wu, Jia-Qi Wang y Nan Zheng. "Metabolomic Analysis Reveals the Mechanisms of Hepatotoxicity Induced by Aflatoxin M1 and Ochratoxin A". Toxins 14, n.º 2 (15 de febrero de 2022): 141. http://dx.doi.org/10.3390/toxins14020141.

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Aflatoxin M1 (AFM1) is the only toxin with the maximum residue limit in milk, and ochratoxin A (OTA) represents a common toxin in cereals foods. It is common to find the co-occurrence of these two toxins in the environment. However, the interactive effect of these toxins on hepatoxicity and underlying mechanisms is still unclear. The liver and serum metabolomics in mice exposed to individual AFM1 at 3.5 mg/kg b.w., OTA at 3.5 mg/kg b.w., and their combination for 35 days were conducted based on the UPLC-MS method in the present study. Subsequent metabolome on human hepatocellular liver carcinoma (Hep G2) cells was conducted to narrow down the key metabolites. The phenotypic results on liver weight and serum indicators, such as total bilirubin and glutamyltransferase, showed that the combined toxins had more serious adverse effects than an individual one, indicating that the combined AFM1 and OTA displayed synergistic effects on liver damage. Through the metabolic analysis in liver and serum, we found that (i) a synergistic effect was exerted in the combined toxins, because the number of differentially expressed metabolites on combination treatment was higher than the individual toxins, (ii) OTA played a dominant role in the hepatoxicity induced by the combination of AFM1, and OTA and (iii) lysophosphatidylcholines (LysoPCs), more especially, LysoPC (16:1), were identified as the metabolites most affected by AFM1 and OTA. These findings provided a new insight for identifying the potential biomarkers for the hepatoxicity of AFM1 and OTA.

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Vannabhum, Manmas, Kamontip Harnphadungkit, Pravit Akarasereenont y Sompol Tapechum. "Untargeted Metabolomics Analysis using LC-MSQTOF for Metabolite Profile Comparison between Patients with Myofascial Pain of Upper Trapezius Muscle versus Controls". Siriraj Medical Journal 74, n.º 11 (1 de noviembre de 2022): 792–803. http://dx.doi.org/10.33192/smj.2022.94.

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Objective: This study aims to identify different biomarkers of Myofascial pain syndrome (MPS) using untargeted metabolomics screening.Materials and Methods: In a case-control study, serum samples from MPS patients (n = 19) and healthy controls (n = 10) were analyzed using reverse-phase liquid chromatography and mass spectrometry quadrupole time-of-flight (MS-QTOF). The resulted raw data was processed with Progenesis QI data analysis software. The HMBD database was used to identify the metabolites based on their fold change (>1.2), variable importance plot (>1) with P < 0.05. MetaboAnalyst 5.0 was used to generate metabolic network analysis for all identified metabolites.Results: The MPS group reported significantly higher pain on visual analog scale when compared with control while most of the other routine blood chemical profiles were not different. Twenty-seven metabolites were analyzed and identified with untargeted metabolomics analysis which could distinguish MPS patients from healthy controls. Inosine and chenodeoxycholic acid were abundant in the MPS group, whereas the others were low. Metabolites were divided into three categories: lipids, nucleotides, and organic compounds. Possible MPS metabolites included lysoSM (sphingomyelin), lysoPC (lysophosphatidylcholine), lysoPE (lysophosphatidylethanolamine), triglyceride, and inosine.Conclusion: These metabolite profiles, including glycerophospholipids mechanism and purine metabolism, indicate that the inflammatory process might be related to the mechanisms of MPS. A larger sample size, a different trigger point location, and modifications in therapy afterward should all be further explored.

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Naz, Shama, Johan Kolmert, Mingxing Yang, Stacey N. Reinke, Muhammad Anas Kamleh, Stuart Snowden, Tina Heyder et al. "Metabolomics analysis identifies sex-associated metabotypes of oxidative stress and the autotaxin–lysoPA axis in COPD". European Respiratory Journal 49, n.º 6 (junio de 2017): 1602322. http://dx.doi.org/10.1183/13993003.02322-2016.

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Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease and a leading cause of mortality and morbidity worldwide. The aim of this study was to investigate the sex dependency of circulating metabolic profiles in COPD.Serum from healthy never-smokers (healthy), smokers with normal lung function (smokers), and smokers with COPD (COPD; Global Initiative for Chronic Obstructive Lung Disease stages I–II/A–B) from the Karolinska COSMIC cohort (n=116) was analysed using our nontargeted liquid chromatography–high resolution mass spectrometry metabolomics platform.Pathway analyses revealed that several altered metabolites are involved in oxidative stress. Supervised multivariate modelling showed significant classification of smokers from COPD (p=2.8×10−7). Sex stratification indicated that the separation was driven by females (p=2.4×10−7) relative to males (p=4.0×10−4). Significantly altered metabolites were confirmed quantitatively using targeted metabolomics. Multivariate modelling of targeted metabolomics data confirmed enhanced metabolic dysregulation in females with COPD (p=3.0×10−3) relative to males (p=0.10). The autotaxin products lysoPA (16:0) and lysoPA (18:2) correlated with lung function (forced expiratory volume in 1 s) in males with COPD (r=0.86; p<0.0001), but not females (r=0.44; p=0.15), potentially related to observed dysregulation of the miR-29 family in the lung.These findings highlight the role of oxidative stress in COPD, and suggest that sex-enhanced dysregulation in oxidative stress, and potentially the autotaxin–lysoPA axis, are associated with disease mechanisms and/or prevalence.

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