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phosphatidic acid/hypoxie

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Protection of neuroblastoma Neuro2A cells from hypoxia-induced apoptosis by cyclic phosphatidic acid (cPA).

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Cyclic phosphatidic acid (cPA) is a naturally occurring phospholipid mediator with a unique cyclic phosphate ring at the sn-2 and sn-3 positions of its glycerol backbone. We have previously shown that cPA significantly suppresses ischemia-induced delayed neuronal death and the accumulation of glial
Hypoxia-inducible factors (HIF-1/HIF-2) govern the expression of critical genes for cellular adaptation to low oxygen tensions. We have previously reported that the intracellular level of phosphatidic acid (PA) rises in response to hypoxia (1% O(2)). In this report, we have explored whether

Influence of postnatal hypoxia on 32P-labeling of polyphosphoinositides and phosphatidic acid in striatum synaptosomes from rat brain.

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Striatum synaptosomes prepared from adult rats which had been exposed to postnatal hypoxia incorporate 32P-phosphate into phosphatidylinositol-4,5-trisphosphate (PI-4,5-P2) with decreased rate. 32P-incorporation amounted to 57% of the control for PI-4,5-P2 labeling and was slightly diminished for

Effect of hypoxia and dopamine on arachidonic acid metabolism in superior cervical ganglion.

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Superior cervical ganglion (SCG) may play a modulatory role on ventilatory control through its efferent sympathetic fibres, which innervate cells in the carotid bodies. In this study the in vivo effect of acute hypoxia versus normoxia on arachidonic acid (AA) metabolism was investigated in cat SCG.

Fatty acids of rice coleoptiles in air and anoxia.

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The metabolism of lipids, like that of other components, was adversely and strongly affected when rice (Oryza sativa L.) coleoptiles were grown anaerobically. In aerobic coleoptiles, the amounts of total fatty acid, phospholipid, and total lipid per coleoptile increased by 2.5- to 3-fold between
Glucose and glutamine are essential energy metabolites for brain tumor growth and survival under both normoxic and hypoxic conditions. Both metabolites can contribute their carbons to lipid biosynthesis. We used uniformly labeled [(14)C]-U-D-glucose and [(14)C]-U-L-glutamine to examine the profile

[Autolytic changes in serum lipids of normal rats and following acute oxygen deficiency].

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Alterations in content of main classes of lipids and phospholipids were studied in blood serum during autolysis in normal rats and in acute oxygen deficiency. In the control animals the most distinct alterations were found in content of phospholipids, which was decreased down to 1/2 of the initial

[Changes in phospholipids of the brain grey and white matter during in vitro autolysis in rats subjected to acute hypobaric hypoxic hypoxia].

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The development of autolysis in grey brain matter of albino rats was accompanied by desintegration of aminophospholipids with parallel increase of glycerophosphates (GLP) and phosphatidic acids (PA) on early stages of incubation and lysophospholipids (LPL) on later stages. Acute hypobaric hypoxic

The effects of lidocaine and hypoxia on phospholipid biosynthesis in the isolated hamster heart.

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In this study, the effects of lidocaine and hypoxia on the biosynthesis of phospholipids in the hamster heart were examined. Hamster hearts were perfused with [1,3-3H]glycerol under normal and hypoxic conditions, and in the absence or presence of 0.5 mg/mL lidocaine. After perfusion, the

Cerebral phosphoinositide, triacylglycerol and energy metabolism during severe hypoxia and recovery.

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The cerebral concentrations of phosphatidylinositol (PI), phosphatidylinositol 4-phosphate (PIP), phosphatidylinositol 4,5-bisphosphate (PIP2), phosphatidic acid (PA), triacylglycerol (TAG) and free fatty acids (FFA), as well as cerebral metabolites, were measured in rats subjected to 10 min of

Evidence for the involvement of diacylglycerol kinase in the activation of hypoxia-inducible transcription factor 1 by low oxygen tension.

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Hypoxia-inducible factor 1 (HIF-1) induces a gene expression program essential for the cellular adaptation to lowered oxygen environments. The intracellular mechanisms by which hypoxia induces HIF-1 remain poorly understood. Here we show that exposure of various cell types to hypoxia raises the

The effects of post-treatment with lisofylline, a phosphatidic acid generation inhibitor, on sepsis-induced acute lung injury in pigs.

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The effects of lisofylline [(R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine] (LSF), an inhibitor of de novo phosphatidic acid (PA) generation, on sepsis-induced acute lung injury was studied using Hanford minipigs weighing 18 to 25 kg. Sepsis was induced by an intravenous infusion of Pseudomonas

Phosphatidic acid signaling mediates lung cytokine expression and lung inflammatory injury after hemorrhage in mice.

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Because phosphatidic acid (PA) pathway signaling may mediate many basic reactions involving cytokine-dependent responses, we investigated the effects of CT1501R, a functional inhibitor of the enzyme lysophosphatidic acid acyltransferase (LPAAT) which converts lysophosphatidic acid (Lyso-PA) to PA.

Role of diacylglycerol induced by hypoxia in the regulation of HIF-1alpha activity.

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Hypoxia-inducible factor 1 (HIF-1) is a critical transcription factor for the adaptation to lowered oxygen environments. We have previously reported that hypoxia induced phosphatidic acid (PA) accumulation through diacylglycerol kinase (DGK) activity and provided evidence that this PA production

Lipid remodelling plays an important role in wheat (Triticum aestivum) hypoxia stress.

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Membrane lipid remodelling is one of the strategies that plants have developed to combat abiotic stress. In this study, physiological, lipidomic and proteome analyses were conducted to investigate the changes in glycerolipid and phospholipid concentrations in the wheat (Triticum aestivum L.)
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