Role of long-chain acyl-coenzyme A synthetases in the regulation of arachidonic acid metabolism in interleukin 1β-stimulated rat fibroblasts

2014 ◽  
Vol 1841 (1) ◽  
pp. 44-53 ◽  
Author(s):  
Hiroshi Kuwata ◽  
Makiko Yoshimura ◽  
Yuka Sasaki ◽  
Emiko Yoda ◽  
Yoshihito Nakatani ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Coenzyme A ◽  
Arachidonic Acid Metabolism ◽  
Interleukin 1Β ◽  
Chain Acyl ◽  
Rat Fibroblasts ◽  
Acyl Coenzyme A ◽  
Long Chain

Role of very-long-chain acyl-coenzyme A synthetase in X-linked adrenoleukodystrophy

1999 ◽  
Vol 46 (3) ◽  
pp. 409-412 ◽  
Author(s):  
Steven J. Steinberg ◽  
Stephan Kemp ◽  
Lelita T. Braiterman ◽  
Paul A. Watkins
Keyword(s):  
Coenzyme A ◽  
Chain Acyl ◽  
Acyl Coenzyme A ◽  
Long Chain

scholarly journals Acyl Coenzyme A Thioesterase 7 Regulates Neuronal Fatty Acid Metabolism To Prevent Neurotoxicity

2013 ◽  
Vol 33 (9) ◽  
pp. 1869-1882 ◽  
Author(s):  
Jessica M. Ellis ◽  
G. William Wong ◽  
Michael J. Wolfgang
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Coenzyme A ◽  
Neurological Diseases ◽  
Conditional Knockout ◽  
Neurological Dysfunction ◽  
Chain Acyl ◽  
Acyl Coenzyme A ◽  
Long Chain

Numerous neurological diseases are associated with dysregulated lipid metabolism; however, the basic metabolic control of fatty acid metabolism in neurons remains enigmatic. Here we have shown that neurons have abundant expression and activity of the long-chain cytoplasmic acyl coenzyme A (acyl-CoA) thioesterase 7 (ACOT7) to regulate lipid retention and metabolism. Unbiased and targeted metabolomic analysis of fasted mice with a conditional knockout of ACOT7 in the nervous system, Acot7 N−/− , revealed increased fatty acid flux into multiple long-chain acyl-CoA-dependent pathways. The alterations in brain fatty acid metabolism were concomitant with a loss of lean mass, hypermetabolism, hepatic steatosis, dyslipidemia, and behavioral hyperexcitability in Acot7 N − / − mice. These failures in adaptive energy metabolism are common in neurodegenerative diseases. In agreement, Acot7 N − / − mice exhibit neurological dysfunction and neurodegeneration. These data show that ACOT7 counterregulates fatty acid metabolism in neurons and protects against neurotoxicity.

scholarly journals The role of OleA His285 in orchestration of long-chain acyl-coenzyme A substrates

FEBS Letters ◽  
2018 ◽  
Vol 592 (6) ◽  
pp. 987-998 ◽  
Author(s):  
Matthew R. Jensen ◽  
Brandon R. Goblirsch ◽  
Morgan A. Esler ◽  
James K. Christenson ◽  
Fatuma A. Mohamed ◽  
...  
Keyword(s):  
Coenzyme A ◽  
Chain Acyl ◽  
Acyl Coenzyme A ◽  
Long Chain

scholarly journals Mechanism of the control of (Na+ + K+)-ATPase by long-chain acyl coenzyme A

1989 ◽  
Vol 264 (5) ◽  
pp. 2605-2608
Author(s):  
W H Huang ◽  
Y Wang ◽  
A Askari
Keyword(s):  
Coenzyme A ◽  
Chain Acyl ◽  
Acyl Coenzyme A ◽  
Long Chain

ANALYSIS OF LONG-CHAIN ACYL-COENZYME A ESTERS

2012 ◽  
pp. 109-131 ◽  
Author(s):  
Tine Bækdal ◽  
Charlotte Karlskov Schjerling ◽  
Jan Krogh Hansen ◽  
Jens Knudsen
Keyword(s):  
Coenzyme A ◽  
Chain Acyl ◽  
Acyl Coenzyme A ◽  
Coenzyme A Esters ◽  
Long Chain

scholarly journals Calcium ionophore synergizes with bacterial lipopolysaccharides in activating macrophage arachidonic acid metabolism.

1988 ◽  
Vol 167 (2) ◽  
pp. 623-631 ◽  
Author(s):  
A A Aderem ◽  
Z A Cohn
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Calcium Ionophore ◽  
Arachidonic Acid Metabolism ◽  
Ionophore A23187 ◽  
Rapid Release ◽  
Lipoxygenase Products ◽  
Order Of Magnitude ◽  
Bacterial Lipopolysaccharides

LPS, a major component of Gram-negative bacterial cell walls, prime macrophages for greatly enhanced arachidonic acid [20:4] metabolism when the cells are subsequently stimulated. The LPS-primed macrophage has been used as a model system in which to study the role of Ca2+ in the regulation of 20:4 metabolism. The Ca2+ ionophore A23187 (0.1 microM) triggered the rapid release of 20:4 metabolites from LPS-primed macrophages but not from cells not previously exposed to LPS. Macrophages required exposure to LPS for at least 40 min before A23187 became effective as a trigger. A23187 (0.1 microM) also synergized with PMA in activating macrophage 20:4 metabolism. The PMA effect could be distinguished from that of LPS since no preincubation with PMA was required. A23187 greatly increased the amount of lipoxygenase products secreted from LPS-primed macrophages, leukotriene C4 synthesis being increased 150-fold. LPS-primed macrophages, partially permeabilized to Ca2+ with A23187, were used to titrate the Ca2+ concentration dependence of the cyclooxygenase and lipoxygenase pathways. Cyclooxygenase metabolites were detected at an order of magnitude lower Ca2+ concentration than were lipoxygenase products. The data suggest that Ca2+ regulates macrophage 20:4 metabolism at two distinct steps: an increase in intracellular Ca2+ regulates the triggering signal and relatively higher Ca2+ concentrations are required for 5-lipoxygenase activity.

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