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[PMID]:27110687
[Au] Autor:Cash JG; Hui DY
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Metabolic Disease Research Center, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
[Ti] Título:Liver-specific overexpression of LPCAT3 reduces postprandial hyperglycemia and improves lipoprotein metabolic profile in mice.
[So] Source:Nutr Diabetes;6:e206, 2016 Apr 25.
[Is] ISSN:2044-4052
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that group 1B phospholipase A2-mediated absorption of lysophospholipids inhibits hepatic fatty acid ß-oxidation and contributes directly to postprandial hyperglycemia and hyperlipidemia, leading to increased risk of cardiometabolic disease. The current study tested the possibility that increased expression of lysophosphatidylcholine acyltransferase-3 (LPCAT3), an enzyme that converts lysophosphatidylcholine to phosphatidylcholine in the liver, may alleviate the adverse effects of lysophospholipids absorbed after a lipid-glucose mixed meal. The injection of an adenovirus vector harboring the human LPCAT3 gene into C57BL/6 mice increased hepatic LPCAT3 expression fivefold compared with mice injected with a control LacZ adenovirus. Postprandial glucose tolerance tests after feeding these animals with a bolus lipid-glucose mixed meal revealed that LPCAT3 overexpression improved postprandial hyperglycemia and glucose tolerance compared with control mice with LacZ adenovirus injection. Mice with LPCAT3 overexpression also showed reduced very low density lipoprotein production and displayed elevated levels of the metabolic- and cardiovascular-protective large apoE-rich high density lipoproteins in plasma. The mechanism underlying the metabolic benefits of LPCAT3 overexpression was shown to be due to the alleviation of lysophospholipid inhibition of fatty acid ß-oxidation in hepatocytes. Taken together, these results suggest that specific LPCAT3 induction in the liver may be a viable strategy for cardiometabolic disease intervention.
[Mh] Termos MeSH primário: 1-Acilglicerofosfocolina O-Aciltransferase/metabolismo
Regulação da Expressão Gênica
Hiperglicemia/genética
Fígado/enzimologia
Metaboloma
[Mh] Termos MeSH secundário: 1-Acilglicerofosfocolina O-Aciltransferase/genética
Animais
Doenças Cardiovasculares/genética
Doenças Cardiovasculares/prevenção & controle
Modelos Animais de Doenças
Teste de Tolerância a Glucose
Fosfolipases A2 do Grupo IB/genética
Fosfolipases A2 do Grupo IB/metabolismo
Hepatócitos/metabolismo
Seres Humanos
Hiperglicemia/prevenção & controle
Metabolismo dos Lipídeos
Lisofosfatidilcolinas/metabolismo
Masculino
Síndrome Metabólica/genética
Síndrome Metabólica/prevenção & controle
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Fosfatidilcolinas/metabolismo
Período Pós-Prandial
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Lysophosphatidylcholines); 0 (Phosphatidylcholines); 0 (Triglycerides); EC 2.3.1.23 (1-Acylglycerophosphocholine O-Acyltransferase); EC 2.3.1.23 (LPCAT3 protein, human); EC 3.1.1.4 (Group IB Phospholipases A2)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160426
[St] Status:MEDLINE
[do] DOI:10.1038/nutd.2016.12


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[PMID]:26872838
[Au] Autor:Nguyen HT; Kim SY; Cho KM; Hong JC; Shin JS; Kim HJ
[Ad] Endereço:Division of Life Sciences, Korea University, Seoul 136-701, Korea.
[Ti] Título:A Transcription Factor γMYB1 Binds to the P1BS cis-Element and Activates PLA2-γ Expression with its Co-Activator γMYB2.
[So] Source:Plant Cell Physiol;57(4):784-97, 2016 Apr.
[Is] ISSN:1471-9053
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Phospholipase A2(PLA2) hydrolyzes phospholipid molecules to produce two products that are both precursors of second messengers of signaling pathways and signaling molecules per se.Arabidopsis thaliana PLA2 paralogs (-ß,-γ and -δ) play critical roles during pollen development, pollen germination and tube growth. In this study, analysis of the PLA2-γ promoter using a deletion series revealed that the promoter region -153 to -1 is crucial for its pollen specificity. Using a yeast one-hybrid screening assay with the PLA2-γ promoter and an Arabidopsis transcription factor (TF)-only library, we isolated two novel MYB-like TFs belonging to the MYB-CC family, denoted here as γMYB1 and γMYB2. By electrophoretic mobility shift assay, we found that these two TFs bind directly to the P1BS (phosphate starvation response 1-binding sequence)cis-element of the PLA2-γ promoter. γMYB1 alone functioned as a transcriptional activator for PLA2-γ expression, whereas γMYB2 directly interacted with γMYB1 and enhanced its activation. Overexpression of γMYB1 in the mature pollen grain led to increased expression of not only the PLA2-γ gene but also of several genes whose promoters contain the P1BS cis-element and which are involved in the Pi starvation response, phospholipid biosynthesis and sugar synthesis. Based on these results, we suggest that the TF γMYB1 binds to the P1BS cis-element, activates the expression of PLA2-γ with the assistance of its co-activator, γMYB2, and regulates the expression of several target genes involved in many plant metabolic reactions.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/metabolismo
Fosfolipases A2 do Grupo IB/metabolismo
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Arabidopsis/genética
Proteínas de Arabidopsis/genética
Sítios de Ligação
Núcleo Celular/metabolismo
Regulação da Expressão Gênica de Plantas
Fosfolipases A2 do Grupo IB/genética
Plantas Geneticamente Modificadas
Pólen/genética
Regiões Promotoras Genéticas
Elementos de Resposta
Transativadores/genética
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (Trans-Activators); 0 (Transcription Factors); 0 (gammaMYB1 protein, Arabidopsis); 0 (gammaMYB2 protein, Arabidopsis); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (phospholipase A2 gamma, Arabidopsis)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170107
[Lr] Data última revisão:
170107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160214
[St] Status:MEDLINE
[do] DOI:10.1093/pcp/pcw024


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[PMID]:25646365
[Au] Autor:Navab M; Chattopadhyay A; Hough G; Meriwether D; Fogelman SI; Wagner AC; Grijalva V; Su F; Anantharamaiah GM; Hwang LH; Faull KF; Reddy ST; Fogelman AM
[Ad] Endereço:Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, CA 90095-1736.
[Ti] Título:Source and role of intestinally derived lysophosphatidic acid in dyslipidemia and atherosclerosis.
[So] Source:J Lipid Res;56(4):871-87, 2015 Apr.
[Is] ISSN:1539-7262
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that i) a Western diet increased levels of unsaturated lysophosphatidic acid (LPA) in small intestine and plasma of LDL receptor null (LDLR(-/-)) mice, and ii) supplementing standard mouse chow with unsaturated (but not saturated) LPA produced dyslipidemia and inflammation. Here we report that supplementing chow with unsaturated (but not saturated) LPA resulted in aortic atherosclerosis, which was ameliorated by adding transgenic 6F tomatoes. Supplementing chow with lysophosphatidylcholine (LysoPC) 18:1 (but not LysoPC 18:0) resulted in dyslipidemia similar to that seen on adding LPA 18:1 to chow. PF8380 (a specific inhibitor of autotaxin) significantly ameliorated the LysoPC 18:1-induced dyslipidemia. Supplementing chow with LysoPC 18:1 dramatically increased the levels of unsaturated LPA species in small intestine, liver, and plasma, and the increase was significantly ameliorated by PF8380 indicating that the conversion of LysoPC 18:1 to LPA 18:1 was autotaxin dependent. Adding LysoPC 18:0 to chow increased levels of LPA 18:0 in small intestine, liver, and plasma but was not altered by PF8380 indicating that conversion of LysoPC 18:0 to LPA 18:0 was autotaxin independent. We conclude that i) intestinally derived unsaturated (but not saturated) LPA can cause atherosclerosis in LDLR(-/-) mice, and ii) autotaxin mediates the conversion of unsaturated (but not saturated) LysoPC to LPA.
[Mh] Termos MeSH primário: Aterosclerose/metabolismo
Dislipidemias/metabolismo
Intestinos/metabolismo
Lisofosfolipídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Aorta/efeitos dos fármacos
Aterosclerose/sangue
Aterosclerose/induzido quimicamente
Benzoxazóis/farmacologia
Gorduras na Dieta/efeitos adversos
Dislipidemias/sangue
Dislipidemias/induzido quimicamente
Feminino
Fosfolipases A2 do Grupo IB/metabolismo
Absorção Intestinal/efeitos dos fármacos
Intestinos/efeitos dos fármacos
Jejuno/efeitos dos fármacos
Jejuno/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Lisofosfatidilcolinas/farmacologia
Lisofosfolipídeos/química
Lisofosfolipídeos/farmacologia
Masculino
Camundongos
Diester Fosfórico Hidrolases/metabolismo
Piperazinas/farmacologia
Receptores de LDL/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (6-(3-(piperazin-1-yl)propanoyl)benzo(d)oxazol-2(3H)-one); 0 (Benzoxazoles); 0 (Dietary Fats); 0 (Lysophosphatidylcholines); 0 (Lysophospholipids); 0 (Piperazines); 0 (Receptors, LDL); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (Pla2g1b protein, mouse); EC 3.1.4.- (Phosphoric Diester Hydrolases); EC 3.1.4.39 (alkylglycerophosphoethanolamine phosphodiesterase); PG6M3969SG (lysophosphatidic acid)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150204
[St] Status:MEDLINE
[do] DOI:10.1194/jlr.M056614


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[PMID]:25335547
[Au] Autor:Pan Y; Wan J; Liu Y; Yang Q; Liang W; Singhal PC; Saleem MA; Ding G
[Ad] Endereço:Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
[Ti] Título:sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor.
[So] Source:Sci Rep;4:6660, 2014 Oct 22.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The M-type phospholipase A2 receptor (PLA2R) is expressed in podocytes in human glomeruli. Group IB secretory phospholipase A2 (sPLA2 IB), which is one of the ligands of the PLA2R, is more highly expressed in chronic renal failure patients than in controls. However, the roles of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are unknown. In the present study, we found that more podocyte apoptosis occurs in the kidneys of patients with higher PLA2R and serum sPLA2 IB levels. In vitro, we demonstrated that human podocyte cells expressed the PLA2R in the cell membrane. After binding with the PLA2R, sPLA2 IB induced podocyte apoptosis in a time- and concentration-dependent manner. sPLA2 IB-induced podocyte PLA2R upregulation was not only associated with increased ERK1/2 and cPLA2α phosphorylation but also displayed enhanced apoptosis. In contrast, PLA2R-silenced human podocytes displayed attenuated apoptosis. sPLA2 IB enhanced podocyte arachidonic acid (AA) content in a dose-dependent manner. These data indicate that sPLA2 IB has the potential to induce human podocyte apoptosis via binding to the PLA2R. The sPLA2 IB-PLA2R interaction stimulated podocyte apoptosis through activating ERK1/2 and cPLA2α and through increasing the podocyte AA content.
[Mh] Termos MeSH primário: Apoptose/genética
Fosfolipases A2 do Grupo IB/biossíntese
Rim/metabolismo
Podócitos/metabolismo
Receptores da Fosfolipase A2/biossíntese
[Mh] Termos MeSH secundário: Adulto
Idoso
Ácido Araquidônico/metabolismo
Biópsia
Feminino
Regulação Enzimológica da Expressão Gênica
Fosfolipases A2 do Grupo IB/metabolismo
Seres Humanos
Rim/patologia
Sistema de Sinalização das MAP Quinases/genética
Masculino
Meia-Idade
Fosforilação
Ligação Proteica
Receptores da Fosfolipase A2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (PLA2R1 protein, human); 0 (Receptors, Phospholipase A2); 27YG812J1I (Arachidonic Acid); EC 3.1.1.4 (Group IB Phospholipases A2)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141023
[St] Status:MEDLINE
[do] DOI:10.1038/srep06660


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[PMID]:25119545
[Au] Autor:Bacha AB
[Ad] Endereço:Biochemistry Department, Science College, King Saud University, P.O Box 22452, Riyadh, 11495, Saudi Arabia. aalghanouchi@ksu.edu.sa.
[Ti] Título:Anti-bactericidal properties of stingray Dasyatis pastinaca groups V, IIA, and IB phospholipases A2: a comparative study.
[So] Source:Appl Biochem Biotechnol;174(4):1520-1534, 2014 Oct.
[Is] ISSN:1559-0291
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Group IIA secreted phospholipase A2 (group IIA sPLA2) is known to display potent Gram-positive bactericidal activity in vitro and in vivo. We have analyzed the bactericidal activity of the full set of native stingray and dromedary groups V, IIA, and IB sPLA2s on several Gram-positive and Gram-negative strains. The rank order potency among both marine and mammal sPLA2s against Gram-positive bacteria is group IIA > V > IB, whereas Gram-negative bacteria exhibited a much higher resistance. There is a synergic action of the sPLA2 with lysozyme when added to the bacteria culture prior to sPLA2.The bactericidal efficiency of groups V and IIA sPLA2s was shown to be dependent upon the presence of calcium ions and to a less extent Mg(2+) ions and then a correlation could be made to its hydrolytic activity of membrane phospholipids. Importantly, we showed that stingray and dromedary groups V, IIA, and IB sPLA2s present no cytotoxicity after their incubation with MDA-MB-231cells. stingray groups V and IIA sPLA2s, like mammal ones, may be considered as future therapeutic agents against bacterial infections.
[Mh] Termos MeSH primário: Antibacterianos/química
Proteínas de Peixes/química
Peixes/metabolismo
Bactérias Gram-Positivas/crescimento & desenvolvimento
Fosfolipases A2 do Grupo IB/química
Fosfolipases A2 do Grupo II/química
Fosfolipases A2 do Grupo V/química
[Mh] Termos MeSH secundário: Animais
Antibacterianos/farmacologia
Cálcio/química
Cálcio/metabolismo
Membrana Celular/química
Membrana Celular/metabolismo
Proteínas de Peixes/farmacologia
Fosfolipases A2 do Grupo IB/farmacologia
Fosfolipases A2 do Grupo II/farmacologia
Fosfolipases A2 do Grupo V/farmacologia
Magnésio/química
Magnésio/metabolismo
Fosfolipídeos/química
Fosfolipídeos/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Fish Proteins); 0 (Phospholipids); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (Group II Phospholipases A2); EC 3.1.1.4 (Group V Phospholipases A2); I38ZP9992A (Magnesium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:170603
[Lr] Data última revisão:
170603
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140815
[St] Status:MEDLINE
[do] DOI:10.1007/s12010-014-1069-x


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[PMID]:24747111
[Au] Autor:Hollie NI; Konaniah ES; Goodin C; Hui DY
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA.
[Ti] Título:Group 1B phospholipase A2 inactivation suppresses atherosclerosis and metabolic diseases in LDL receptor-deficient mice.
[So] Source:Atherosclerosis;234(2):377-80, 2014 Jun.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Previous studies have shown that inactivation of the group 1B phospholipase A2 (Pla2g1b) suppresses diet-induced obesity, hyperglycemia, insulin resistance, and hyperlipidemia in C57BL/6 mice. A possible influence of Pla2g1b inactivation on atherosclerosis has not been addressed previously. The current study utilized LDL receptor-deficient (Ldlr(-/-)) mice with plasma lipid levels and distribution similar to hyperlipidemic human subjects as a preclinical animal model to test the effectiveness of Pla2g1b inactivation on atherosclerosis. METHODS AND RESULTS: The Pla2g1b(+/+)Ldlr(-/-) and Pla2g1b(-/-)Ldlr(-/-) mice were fed a low fat chow diet or a hypercaloric diet with 58.5 kcal% fat and 25 kcal% sucrose for 10 weeks. Minimal differences were observed between Pla2g1b(+/+)Ldlr(-/-) and Pla2g1b(-/-)Ldlr(-/-) mice when the animals were maintained on the low fat chow diet. However, when the animals were maintained on the hypercaloric diet, the Pla2g1(+/+)Ldlr(-/-) mice showed the expected body weight gain but the Pla2g1b(-/-)Ldlr(-/-) mice were resistant to diet-induced body weight gain. The Pla2g1b(-/-)Ldlr(-/-) mice also displayed lower fasting glucose, insulin, and plasma lipid levels compared to the Pla2g1b(+/+)Ldlr(-/-) mice, which displayed robust hyperglycemia, hyperinsulinemia, and hyperlipidemia in response to the hypercaloric diet. Importantly, atherosclerotic lesions in the aortic roots were also reduced 7-fold in the Pla2g1b(-/-)Ldlr(-/-) mice. CONCLUSION: The effectiveness of Pla2g1b inactivation to suppress diet-induced body weight gain and reduce diabetes and atherosclerosis in LDL receptor-deficient mice suggests that pharmacological inhibition of Pla2g1b may be a viable strategy to decrease diet-induced obesity and the risk of diabetes and atherosclerosis in humans.
[Mh] Termos MeSH primário: Aterosclerose/prevenção & controle
Fosfolipases A2 do Grupo IB/deficiência
Hiperglicemia/prevenção & controle
Hiperinsulinismo/prevenção & controle
Hiperlipidemias/prevenção & controle
Receptores de LDL/deficiência
[Mh] Termos MeSH secundário: Animais
Aterosclerose/sangue
Aterosclerose/enzimologia
Aterosclerose/genética
Biomarcadores/sangue
Glicemia/metabolismo
Gorduras na Dieta
Modelos Animais de Doenças
Ingestão de Energia
Fosfolipases A2 do Grupo IB/genética
Hiperglicemia/sangue
Hiperglicemia/enzimologia
Hiperglicemia/genética
Hiperinsulinismo/sangue
Hiperinsulinismo/enzimologia
Hiperinsulinismo/genética
Hiperlipidemias/sangue
Hiperlipidemias/enzimologia
Hiperlipidemias/genética
Insulina/sangue
Lipídeos/sangue
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de LDL/genética
Ganho de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Dietary Fats); 0 (Insulin); 0 (Lipids); 0 (Receptors, LDL); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (Pla2g1b protein, mouse)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:170120
[Lr] Data última revisão:
170120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140422
[St] Status:MEDLINE


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[PMID]:24114173
[Au] Autor:Varga A; Jenes A; Marczylo TH; Sousa-Valente J; Chen J; Austin J; Selvarajah S; Piscitelli F; Andreou AP; Taylor AH; Kyle F; Yaqoob M; Brain S; White JP; Csernoch L; Di Marzo V; Buluwela L; Nagy I
[Ad] Endereço:Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, 369 Fulham Road, London, SW10 9NH, UK.
[Ti] Título:Anandamide produced by Ca(2+)-insensitive enzymes induces excitation in primary sensory neurons.
[So] Source:Pflugers Arch;466(7):1421-35, 2014 Jul.
[Is] ISSN:1432-2013
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The endogenous lipid agent N-arachidonoylethanolamine (anandamide), among other effects, has been shown to be involved in nociceptive processing both in the central and peripheral nervous systems. Anandamide is thought to be synthesised by several enzymatic pathways both in a Ca(2+)-sensitive and Ca(2+)-insensitive manner, and rat primary sensory neurons produce anandamide. Here, we show for the first time, that cultured rat primary sensory neurons express at least four of the five known Ca(2+)-insensitive enzymes implicated in the synthesis of anandamide, and that application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl, the common substrate of the anandamide-synthesising pathways, results in anandamide production which is not changed by the removal of extracellular Ca(2+). We also show that anandamide, which has been synthesised in primary sensory neurons following the application of 1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl induces a transient receptor potential vanilloid type 1 ion channel-mediated excitatory effect that is not inhibited by concomitant activation of the cannabinoid type 1 receptor. Finally, we show that sub-populations of transient receptor potential vanilloid type 1 ion channel-expressing primary sensory neurons also express some of the putative Ca(2+)-insensitive anandamide-synthesising enzymes. Together, these findings indicate that anandamide synthesised by primary sensory neuron via a Ca(2+)-insensitive manner has an excitatory rather than an inhibitory role in primary sensory neurons and that excitation is mediated predominantly through autocrine signalling. Regulation of the activity of the Ca(2+)-insensitive anandamide-synthesising enzymes in these neurons may be capable of regulating the activity of these cells, with potential relevance to controlling nociceptive processing.
[Mh] Termos MeSH primário: Potenciais de Ação
Ácidos Araquidônicos/metabolismo
Cálcio/metabolismo
Endocanabinoides/metabolismo
Fosfatidiletanolaminas/farmacologia
Alcamidas Poli-Insaturadas/metabolismo
Células Receptoras Sensoriais/metabolismo
[Mh] Termos MeSH secundário: Animais
Ácidos Araquidônicos/biossíntese
Células Cultivadas
Endocanabinoides/biossíntese
Gânglios Espinais/citologia
Gânglios Espinais/enzimologia
Gânglios Espinais/metabolismo
Fosfolipases A2 do Grupo IB/genética
Fosfolipases A2 do Grupo IB/metabolismo
Lisofosfolipase/genética
Lisofosfolipase/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fosfatidiletanolaminas/química
Diester Fosfórico Hidrolases/genética
Diester Fosfórico Hidrolases/metabolismo
Proteína Tirosina Fosfatase não Receptora Tipo 22/genética
Proteína Tirosina Fosfatase não Receptora Tipo 22/metabolismo
Ratos
Ratos Sprague-Dawley
Células Receptoras Sensoriais/enzimologia
Células Receptoras Sensoriais/fisiologia
Canais de Cátion TRPV/genética
Canais de Cátion TRPV/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1,2-dioleoyl-sn-glycero-3-phosphoethanolamine-N-arachidonoyl); 0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Phosphatidylethanolamines); 0 (Polyunsaturated Alkamides); 0 (TRPV Cation Channels); 0 (TRPV1 protein, mouse); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.5 (Lysophospholipase); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 22); EC 3.1.4.- (Phosphoric Diester Hydrolases); EC 3.1.4.46 (glycerophosphodiester phosphodiesterase); SY7Q814VUP (Calcium); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131012
[St] Status:MEDLINE
[do] DOI:10.1007/s00424-013-1360-7


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[PMID]:24120965
[Au] Autor:Ben Bacha A; Abid I; Horchani H; Mejdoub H
[Ad] Endereço:Biochemistry Department, Science College, King Saud University, P.O. Box 22452, Riyadh 11495, Saudi Arabia; Laboratory of Plant Biotechnology Applied to Crop Improvement, Faculty of Science of Sfax, University of Sfax, Sfax 3038, Tunisia. Electronic address: abirghanouchibenbacha@yahoo.fr.
[Ti] Título:Enzymatic properties of stingray Dasyatis pastinaca group V, IIA and IB phospholipases A(2): a comparative study.
[So] Source:Int J Biol Macromol;62:537-42, 2013 Nov.
[Is] ISSN:1879-0003
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In the present study, we have purified the group V phospholipase from the heart of cartilaginous fish stingray Dasyatis pastinaca and compared its biochemical properties with group IIA (sPLA2-IIA) and IB (sPLA2-IB) phospholipases previously purified from pancreas and intestine, respectively. Group V phospholipase (sPLA2-V) was purified to homogeneity by heat treatment, ammonium sulphate precipitation and RP-HPLC. The N-terminal sequence of the purified sPLA2-V exhibits a high degree of homology with those of mammal. The enzyme was found to be monomeric with a molecular mass estimation of 14 kDa. The specific activity of the purified enzyme, measured at pH 8 and 37 °C was 52 U/mg. Like sPLA2-IB and sPLA2-IIA, the sPLA2-V is found to be stable between pH 3 and 11 after 30 min of incubation. The purified sPLA2-V retained 65% of its activity after 10 min of incubation at 70 °C and it absolutely requires Ca(2+) for enzymatic activity. In addition it displayed high tolerance to organic solvents. Kinetic parameters Kmapp, kcat and the deduced catalytic efficiency (kcat/Kmapp) of the purified group-V, -IB and -IIA PLA2s were determined using phosphatidylethanolamine (PE), phosphatidylcholine (PC) or phosphatidylserine (PS) as substrate. The three enzymes hydrolyze the zwiterionic PE and PC substrates more efficiently than anionic PS substrate.
[Mh] Termos MeSH primário: Elasmobrânquios/metabolismo
Fosfolipases A2 do Grupo IB/metabolismo
Fosfolipases A2 do Grupo II/metabolismo
Fosfolipases A2 do Grupo V/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Ácidos e Sais Biliares/farmacologia
Cálcio/química
Cálcio/farmacologia
Ativação Enzimática/efeitos dos fármacos
Fosfolipases A2 do Grupo IB/química
Fosfolipases A2 do Grupo II/química
Fosfolipases A2 do Grupo V/química
Fosfolipases A2 do Grupo V/isolamento & purificação
Concentração de Íons de Hidrogênio
Cinética
Dados de Sequência Molecular
Alinhamento de Sequência
Solventes
Especificidade por Substrato
Temperatura Ambiente
Tripsina/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bile Acids and Salts); 0 (Solvents); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (Group II Phospholipases A2); EC 3.1.1.4 (Group V Phospholipases A2); EC 3.4.21.4 (Trypsin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:131122
[Lr] Data última revisão:
131122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131015
[St] Status:MEDLINE


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[PMID]:23874843
[Au] Autor:Matsumoto Y; Matsuura T; Aoyagi H; Matsuda M; Hmwe SS; Date T; Watanabe N; Watashi K; Suzuki R; Ichinose S; Wake K; Suzuki T; Miyamura T; Wakita T; Aizaki H
[Ad] Endereço:Department of Virology II, National Institute of Infectious Diseases, Tokyo, Japan.
[Ti] Título:Antiviral activity of glycyrrhizin against hepatitis C virus in vitro.
[So] Source:PLoS One;8(7):e68992, 2013.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glycyrrhizin (GL) has been used in Japan to treat patients with chronic viral hepatitis, as an anti-inflammatory drug to reduce serum alanine aminotransferase levels. GL is also known to exhibit various biological activities, including anti-viral effects, but the anti-hepatitis C virus (HCV) effect of GL remains to be clarified. In this study, we demonstrated that GL treatment of HCV-infected Huh7 cells caused a reduction of infectious HCV production using cell culture-produced HCV (HCVcc). To determine the target step in the HCV lifecycle of GL, we used HCV pseudoparticles (HCVpp), replicon, and HCVcc systems. Significant suppressions of viral entry and replication steps were not observed. Interestingly, extracellular infectivity was decreased, and intracellular infectivity was increased. By immunofluorescence and electron microscopic analysis of GL treated cells, HCV core antigens and electron-dense particles had accumulated on endoplasmic reticulum attached to lipid droplet (LD), respectively, which is thought to act as platforms for HCV assembly. Furthermore, the amount of HCV core antigen in LD fraction increased. Taken together, these results suggest that GL inhibits release of infectious HCV particles. GL is known to have an inhibitory effect on phospholipase A2 (PLA2). We found that group 1B PLA2 (PLA2G1B) inhibitor also decreased HCV release, suggesting that suppression of virus release by GL treatment may be due to its inhibitory effect on PLA2G1B. Finally, we demonstrated that combination treatment with GL augmented IFN-induced reduction of virus in the HCVcc system. GL is identified as a novel anti-HCV agent that targets infectious virus particle release.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Ácido Glicirrízico/farmacologia
Hepacivirus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células
Linhagem Celular
Eletroporação
Retículo Endoplasmático/metabolismo
Técnica Indireta de Fluorescência para Anticorpo
Fosfolipases A2 do Grupo IB/metabolismo
Seres Humanos
Microscopia Eletrônica de Transmissão
Interferência de RNA
Internalização do Vírus/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 6FO62043WK (Glycyrrhizic Acid); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (PLA2G1B protein, human)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:150423
[Lr] Data última revisão:
150423
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130723
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0068992


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[PMID]:23817419
[Au] Autor:Tamaru S; Mishina H; Watanabe Y; Watanabe K; Fujioka D; Takahashi S; Suzuki K; Nakamura T; Obata JE; Kawabata K; Yokota Y; Murakami M; Hanasaki K; Kugiyama K
[Ad] Endereço:Department of Internal Medicine II, Faculty of Medicine, University of Yamanashi, Chuo, Yamanashi 409-3898, Japan.
[Ti] Título:Deficiency of phospholipase A2 receptor exacerbates ovalbumin-induced lung inflammation.
[So] Source:J Immunol;191(3):1021-8, 2013 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Secretory phospholipase A2 (sPLA2) plays a critical role in the genesis of lung inflammation through proinflammatory eicosanoids. A previous in vitro experiment showed a possible role of cell surface receptor for sPLA2 (PLA2R) in the clearance of extracellular sPLA2. PLA2R and groups IB and X sPLA2 are expressed in the lung. This study examined a pathogenic role of PLA2R in airway inflammation using PLA2R-deficient (PLA2R(-/-)) mice. Airway inflammation was induced by immunosensitization with OVA. Compared with wild-type (PLA2R(+/+)) mice, PLA2R(-/-) mice had a significantly greater infiltration of inflammatory cells around the airways, higher levels of groups IB and X sPLA2, eicosanoids, and Th2 cytokines, and higher numbers of eosinophils and neutrophils in bronchoalveolar lavage fluid after OVA treatment. In PLA2R(-/-) mice, intratracheally instilled [(125)I]-labeled sPLA2-IB was cleared much more slowly from bronchoalveolar lavage fluid compared with PLA2R(+/+) mice. The degradation of the instilled [(125)I]-labeled sPLA2-IB, as assessed by trichloroacetic acid-soluble radioactivity in bronchoalveolar lavage fluid after instillation, was lower in PLA2R(-/-) mice than in PLA2R(+/+) mice. In conclusion, PLA2R deficiency increased sPLA2-IB and -X levels in the lung through their impaired clearance from the lung, leading to exaggeration of lung inflammation induced by OVA treatment in a murine model.
[Mh] Termos MeSH primário: Fosfolipases A2 do Grupo IB/metabolismo
Fosfolipases A2 do Grupo X/metabolismo
Pneumonia/imunologia
Receptores da Fosfolipase A2/genética
Receptores da Fosfolipase A2/metabolismo
[Mh] Termos MeSH secundário: Animais
Líquido da Lavagem Broncoalveolar/citologia
Eicosanoides/metabolismo
Eosinófilos/imunologia
Feminino
Fosfolipases A2 do Grupo IB/imunologia
Fosfolipases A2 do Grupo X/imunologia
Pulmão/imunologia
Pulmão/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Neutrófilos/imunologia
Ovalbumina/imunologia
Pneumonia/genética
Receptores da Fosfolipase A2/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Eicosanoids); 0 (Receptors, Phospholipase A2); 9006-59-1 (Ovalbumin); EC 3.1.1.4 (Group IB Phospholipases A2); EC 3.1.1.4 (Group X Phospholipases A2); EC 3.1.1.4 (Pla2g10 protein, mouse); EC 3.1.1.4 (Pla2g1b protein, mouse)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:130722
[Lr] Data última revisão:
130722
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:130703
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1300738



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