Phospholipases and acyltransferases in macrophages

Flesch, I; Schonhardt, T.; Ferber, E.

doi:10.1007/bf01711335

Cited by 13 publications

(6 citation statements)

References 15 publications

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“…It has traditionally been assumed that PL AA incorporation in activated cells may be secondary to the PLA 2 hydrolytic step because AA incorporates preferentially into the sn-2 position of PLs, and thus, for an enhanced AA reacylation to occur, 2-lysophospholipid acceptors, produced only by PLA 2 , should be provided. That lysophospholipid availability may limit AA reacylation in activated cells is also inferred from the finding that the specific activities of the enzymes of the reacylation pathway, ACSL and the CoA-dependent acyltransferases, are severalfold higher that that of PLA 2 in homogenates from resting and activated cells (23,(54)(55)(56)(57)(58).…”

Section: Discussionmentioning

confidence: 98%

Signaling Role for Lysophosphatidylcholine Acyltransferase 3 in Receptor-Regulated Arachidonic Acid Reacylation Reactions in Human Monocytes

Pérez-Chacón

Astudillo²,

Ruipérez³

et al. 2009

The Journal of Immunology

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Cellular availability of free arachidonic acid (AA) is an important step in the production of pro- and anti-inflammatory eicosanoids. Control of free AA levels in cells is carried out by the action of phospholipase A2s and lysophospholipid acyltransferases, which are responsible for the reactions of deacylation and incorporation of AA from and into the sn-2 position of phospholipids, respectively. In this work, we have examined the pathways for AA incorporation into phospholipids in human monocytes stimulated by zymosan. Our data show that stimulated cells exhibit an enhanced incorporation of AA into phospholipids that is not secondary to an increased availability of lysophospholipid acceptors due to phospholipase A2 activation but rather reflects the receptor-regulated nature of the AA reacylation pathway. In vitro activity measurements indicate that the receptor-sensitive step of the AA reacylation pathway is the acyltransferase using lysophosphatidylcholine (lysoPC) as acceptor, and inhibition of the enzyme lysoPC acyltransferase 3 by specific small interfering RNA results in inhibition of the stimulated incorporation of AA into phospholipids. Collectively, these results define lysoPC acyltransferase 3 as a novel-signal–regulated enzyme that is centrally implicated in limiting free AA levels in activated cells.

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Section: Discussionmentioning

confidence: 98%

Signaling Role for Lysophosphatidylcholine Acyltransferase 3 in Receptor-Regulated Arachidonic Acid Reacylation Reactions in Human Monocytes

Pérez-Chacón

Astudillo²,

Ruipérez³

et al. 2009

The Journal of Immunology

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“…Adrenic acid is the precursor of 22-carbon 1a,1b-dihomologue prostaglandins (dihomoprostaglandins) [23][24][25][26]. The potent biological activity of the eicosanoids compels the cells to tightly control the leveles of free AA in such a manner that availability of free AA is frequently a rate-limiting step in eicosanoid generation [27,28].…”

Section: Cellular Utilization Of Arachidonic Acidmentioning

confidence: 99%

Dynamics of arachidonic acid mobilization by inflammatory cells

Astudillo¹,

Balgoma²,

Balboa³

et al. 2012

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

107

110

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The development of mass spectrometry-based techniques is opening new insights into the understanding of arachidonic acid (AA) metabolism. AA incorporation, remodeling and release are collectively controlled by acyltransferases, phospholipases and transacylases that exquisitely regulate the distribution of AA between the different glycerophospholipid species and its mobilization during cellular stimulation. Traditionally, studies involving phospholipid AA metabolism were conducted by using radioactive precursors and scintillation counting from thin layer chromatography separations that provided only information about lipid classes. Today, the input of lipidomic approaches offers the possibility of characterizing and quantifying specific molecular species with great accuracy and within a biological context associated to protein and/or gene expression in a temporal frame. This review summarizes recent results applying mass spectrometry-based lipidomic approaches to the identification of AA-containing glycerophospholipids, phospholipid AA remodeling and synthesis of oxygenated metabolites.

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“…Because of the potent biological actions of the eicosanoids cells keep this fatty acid at very low levels, by promoting its esterification into cellular lipids. As a matter of fact the availability of free AA is well described to constitute a rate-limiting step in the generation of eicosanoids by mammalian cells [3,4]. In addition, free AA may also exert signaling functions by itself, e.g.…”

Section: Introductionmentioning

confidence: 99%

Control of free arachidonic acid levels by phospholipases A2 and lysophospholipid acyltransferases

Pérez-Chacón

Astudillo

Balgoma

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

158

190

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Arachidonic acid (AA) and its oxygenated derivatives, collectively known as the eicosanoids, are key mediators of a wide variety of physiological and pathophysiological states. AA, obtained from the diet or synthesized from linoleic acid, is rapidly incorporated into cellular phospholipids by the concerted action of arachidonoyl-CoA synthetase and lysophospholipid acyltransferases. Under the appropriate conditions, AA is liberated from its phospholipid storage sites by the action of one or various phospholipase A(2) enzymes. Thus, cellular availability of AA, and hence the amount of eicosanoids produced, depends on an exquisite balance between phospholipid reacylation and hydrolysis reactions. This review focuses on the enzyme families that are involved in these reactions in resting and stimulated cells.

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Phospholipases and acyltransferases in macrophages

Cited by 13 publications

References 15 publications

Signaling Role for Lysophosphatidylcholine Acyltransferase 3 in Receptor-Regulated Arachidonic Acid Reacylation Reactions in Human Monocytes

Signaling Role for Lysophosphatidylcholine Acyltransferase 3 in Receptor-Regulated Arachidonic Acid Reacylation Reactions in Human Monocytes

Dynamics of arachidonic acid mobilization by inflammatory cells

Control of free arachidonic acid levels by phospholipases A2 and lysophospholipid acyltransferases

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