scholarly journals Neutral Lipids Are Not a Source of Arachidonic Acid for Lipid Mediator Signaling in Human Foamy Monocytes

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 941 ◽  
Author(s):  
Carlos Guijas ◽  
Miguel A. Bermúdez ◽  
Clara Meana ◽  
Alma M. Astudillo ◽  
Laura Pereira ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Neutral Lipids ◽  
Lipid Mediator ◽  
Secretory Product ◽  
Cellular Functions ◽  
Atherosclerotic Lesions ◽  
Free Arachidonic Acid ◽  
Phospholipid Pool ◽  
Stimulation Of

Human monocytes exposed to free arachidonic acid (AA), a secretory product of endothelial cells, acquire a foamy phenotype which is due to the accumulation of cytoplasmic lipid droplets with high AA content. Recruitment of foamy monocytes to the inflamed endothelium contributes to the development of atherosclerotic lesions. In this work, we investigated the potential role of AA stored in the neutral lipids of foamy monocytes to be cleaved by lipases and contribute to lipid mediator signaling. To this end, we used mass spectrometry-based lipidomic approaches combined with strategies to generate monocytes with different concentrations of AA. Results from our experiments indicate that the phospholipid AA pool in monocytes is stable and does not change upon exposure of the cells to the external AA. On the contrary, the AA pool in triacylglycerol is expandable and can accommodate relatively large amounts of fatty acid. Stimulation of the cells with opsonized zymosan results in the expected decreases of cellular AA. Under all conditions examined, all of the AA decreases observed in stimulated cells were accounted for by decreases in the phospholipid pool; we failed to detect any contribution of the triacylglycerol pool to the response. Experiments utilizing selective inhibitors of phospholipid or triacylglyerol hydrolysis confirmed that the phospholipid pool is the sole contributor of the AA liberated by stimulated cells. Thus, the AA in the triacylglycerol is not a source of free AA for the lipid mediator signaling during stimulation of human foamy monocytes and may be used for other cellular functions.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

scholarly journals Role of prostaglandins in hypoxia-stimulated erythropoietin production

1985 ◽  
Vol 249 (1) ◽  
pp. C3-C8 ◽  
Author(s):  
A. Kurtz ◽  
W. Jelkmann ◽  
J. Pfeilschifter ◽  
C. Bauer
Keyword(s):  
Arachidonic Acid ◽  
Adenylate Cyclase ◽  
Cell Cultures ◽  
Mesangial Cells ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Cyclooxygenase Inhibitor ◽  
Erythropoietin Production ◽  
Stimulation Of

The role of prostaglandins in the mediation of hypoxia-stimulated erythropoietin (Ep) production by cultured rat renal mesangial cells was examined. It was found that an increase in prostaglandin E2 (PGE2) production accompanied the rise in Ep due to hypoxia (2% O2). The hypoxia-stimulated increase in Ep production was abolished in the presence of the cyclooxygenase inhibitor indomethacin (10(-5) M). When PGE2 (10(-6) M was added simultaneously with indomethacin, however, no diminution in hypoxia-stimulated Ep production was observed. Addition of arachidonic acid (AA, 10(-5) M), PGE2 (10(-6) M), or PGI2 (10(-4) M) enhanced Ep production under normoxic conditions (20% O2), while PGF2 alpha (10(-6) M) had no effect on Ep production. AA, PGE2, and PGI2 were found to stimulate adenosine 3',5'-cyclic monophosphate formation by the cultured mesangial cells. Enhancement of adenylate cyclase activity by forskolin (10(-5) M) also increased Ep production in the cell cultures. Our results suggest that hypoxia-stimulated Ep production by cultured mesangial cells is mediated by prostaglandins with subsequent stimulation of adenylate cyclase activity.

Oxytocin Signaling Pathway: From Cell Biology To Clinical Implications.

2020 ◽  
Vol 20 ◽  
Author(s):  
Michele Iovino ◽  
Tullio Messana ◽  
Anna Tortora ◽  
Consuelo Giusti ◽  
Giuseppe Lisco ◽  
...  
Keyword(s):  
Cell Biology ◽  
Brain Anatomy ◽  
Clinical Context ◽  
Β Cell ◽  
Atherosclerotic Lesions ◽  
Mesh Terms ◽  
Anti Oxidant ◽  
Psychiatric Conditions ◽  
Stimulation Of

Background: In addition to the well known role played on lactation and parturition, Oxytocin (OT) and OT receptor (OTR) are involved in many other aspects such as the control of maternal and social behavior, the regulation of the growth of the neocortex, the maintenance of blood supply to the cortex, the stimulation of limbic olfactory area to mother-infant recognition bond, and the modulation of the autonomic nervous system via vagal pathway. Moreover, OT and OTR show anti-inflammatory, anti-oxidant, anti-pain, antidiabetic, anti-dyslipidemic and anti-atherogenic effects. Objective: The aim of this narrative review is to summarize the main data coming from the literature dealing with the role of OT and OTR in physiology and pathologic conditions focusing on the most relevant aspects. Methods: Appropriate keywords and MeSH terms were identified and searched in Pubmed. Finally, references of original articles and reviews were examined. Results: We report the most significant and updated data about the role played by OT and OTR in physiology and in different clinical context. Conclusion: Emerging evidence indicates the involvement of OT system in several pathophysiological mechanisms influencing brain anatomy, cognition, language, sense of safety and trust and maternal behavior, with a possible use of exogenous administered OT in the treatment of specific neuro-psychiatric conditions. Furthermore, it modulates pancreatic β-cell responsiveness and lipid metabolism leading to possible therapeutic use in diabetic and dyslipidemic patients and for limiting and even reversing atherosclerotic lesions.

Prostaglandins in adrenergic transmission of isolated perfused rat pancreas.

1977 ◽  
Vol 232 (2) ◽  
pp. E201
Author(s):  
M Hamamdzić ◽  
K U Malik
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin F2alpha ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Isolated Perfused Rat Pancreas ◽  
Adrenergic Transmission ◽  
Vascular Beds ◽  
Neuroeffector Junction ◽  
Stimulation Of

In the isolated, perfused rat pancreas, prostaglandins (PGs) E1 and E2 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2alpha had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicylic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter three agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2alpha inhibited the vasoconstrictor responses to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

Uptake and utilization of arachidonic acid in infective larvae of Angiostrongylus cantonensis

2010 ◽  
Vol 85 (4) ◽  
pp. 395-400 ◽  
Author(s):  
P. Tang ◽  
L.-C. Wang
Keyword(s):  
Arachidonic Acid ◽  
Fatty Acid ◽  
Neutral Lipids ◽  
Scintillation Counting ◽  
Angiostrongylus Cantonensis ◽  
Infective Larvae ◽  
Exogenous Arachidonic Acid ◽  
Lipid Pool ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Phospholipid Pool

AbstractInfective larvae of Angiostrongylus cantonensis may take up and incorporate exogenous arachidonic acid into their lipid pool. By scintillation counting, uptake and incorporation were determined to be time dependent. Arachidonic acid was mainly incorporated into phospholipid (56.8%) and neutral lipid (22.4%) pools. In the neutral lipids, 64.0% was diglyceride and 36.0% triglyceride. Phosphatidylcholine was the predominant fatty acid in the phospholipid pool. In addition to the release of leukotriene B4, the parasite was found to generate radiolabelled CO2 after incubation with [U-14C]arachidonate. Moreover, enzymatic analysis of crude extracts revealed the presence of acyl-CoA dehydrogenase (short and long chain), thiolase, enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase. These findings suggest that infective larvae of A. cantonensis not only take up and incorporate exogenous arachidonic acid into their lipid pool, but may also utilize the fatty acid through a functional β-oxidation pathway.

scholarly journals Protein synthesis in isolated rabbit forelimb muscles. The possible role of metabolites of arachidonic acid in the response to intermittent stretching

1983 ◽  
Vol 214 (1) ◽  
pp. 153-161 ◽  
Author(s):  
R H Smith ◽  
R M Palmer ◽  
P J Reeds
Keyword(s):  
Protein Synthesis ◽  
Arachidonic Acid ◽  
High Concentration ◽  
Constant Tension ◽  
Free Arachidonic Acid ◽  
Intact Rabbit ◽  
Forelimb Muscles ◽  
Mechanical Stretching ◽  
Consequent Increase

Protein synthesis was measured in isolated intact rabbit muscles by the incorporation of [3H]phenylalanine added at a high concentration (2.5 mM) to the incubation medium. Intermittent mechanical stretching substantially increased the rate of protein synthesis relative to that in control muscles incubated under a constant tension. Indomethacin and meclofenamic acid, inhibitors of the enzyme cyclo-oxygenase, which converts free arachidonic acid into the prostaglandins, prostacyclins and thromboxanes, decreased the rate of protein synthesis in intermittently stretched muscles, but had no effect on synthesis rates in the unstimulated controls. Arachidonic acid at concentrations of 0.2 and 1.0 microM gave a highly significant increase in the rate of protein synthesis in muscles incubated under a constant tension. The ability of arachidonic acid to increase protein-synthesis rates was abolished by the addition of indomethacin. Activation of protein synthesis by intermittent stretching persisted for 10-20 min after the stretch stimulation had ceased. Indomethacin, added either during the initial incubation with intermittent stretching or during the subsequent period when protein synthesis was measured after stimulation had ceased, decreased protein-synthesis rates. This decrease was similar whether indomethacin was present during the initial, final or entire incubation period. In experiments analogous with those in (4) above, when Ca2+ was withheld and EGTA added for the entire incubation, rates of protein synthesis were again decreased. The rates of protein synthesis observed when Ca2+ was present during either an initial stimulation phase or a final, unstimulated, measurement phase were similar, and were intermediate between control rates and those in muscles incubated without Ca2+ for the whole experiment. Two prostaglandins, F2 alpha (2.8 microM) and A1 (28 microM), increased rates of protein synthesis in unstimulated muscles, but prostaglandins E2 and D2 and the leukotrienes C4 and D4 failed to do so. It is concluded that the stretch-stimulated increase in protein synthesis may be caused by activation of membrane phospholipases, release of arachidonic acid and a consequent increase in prostaglandin synthesis.

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