|
|
|
|||||||
|
|||||||||
J. Biol. Chem., Vol. 276, Issue 2, 1439-1449, January 12, 2001
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Department of Internal Medicine, Pulmonary and Critical
Care Medicine, Wake Forest University School of Medicine,
Winston-Salem, North Carolina 27154
The goal of this study was to examine arachidonic
acid (AA) metabolism by murine bone marrow-derived mast cells (BMMC)
during apoptosis induced by cytokine depletion. BMMC deprived of
cytokines for 12-48 h displayed apoptotic characteristics. During
apoptosis, levels of AA, but not other unsaturated fatty acids,
correlated with the percentage of apoptotic cells. A decrease in both
cytosolic phospholipase A2 expression and
activity indicated that cytosolic phospholipase A2 did not
account for AA mobilization during apoptosis. Free AA accumulation is
also unlikely to be due to decreases in 5-lipoxygenase and/or
cyclooxygenase activities, since BMMC undergoing apoptosis produced
similar amounts of leukotriene B4 and significantly greater
amounts of PGD2 than control cells. Arachidonoyl-CoA
synthetase and CoA-dependent transferase activities
responsible for incorporating AA into phospholipids were not altered
during apoptosis. However, there was an increase in arachidonate in
phosphatidylcholine (PC) and neutral lipids concomitant with a
40.7 ± 8.1% decrease in arachidonate content in
phosphatidylethanolamine (PE), suggesting a diminished capacity of mast
cells to remodel arachidonate from PC to PE pools. Further evidence of
a decrease in AA remodeling was shown by a significant decrease in
microsomal CoA-independent transacylase activity. Levels of lyso-PC and
lyso-PE were not altered in cells undergoing apoptosis, suggesting that
the accumulation of lysophospholipids did not account for the decrease
in CoA-independent transacylase activity or the induction of apoptosis.
Together, these data suggest that the mole quantities of free AA
closely correlated with apoptosis and that the accumulation of AA in
BMMC during apoptosis was mediated by a decreased capacity of these cells to remodel AA from PC to PE.
A Decrease in Remodeling Accounts for the Accumulation of
Arachidonic Acid in Murine Mast Cells Undergoing Apoptosis*
,,, and§
*
This work was supported in part by National Institutes of
Health Grant AI 24985 SI (to F. A. N.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom all correspondence should be addressed: Dept. of Internal
Medicine, Section on Pulmonary and Critical Care Medicine, Wake Forest
University School of Medicine, Medical Center Blvd., Winston-Salem, NC
27157-1054. Tel.: 336-716-9923; Fax: 336-716-7277; E-mail:
afonteh@wfubmc.edu.
§
Present address: US EPA, 86 TW Alexander Dr., MD 82, Research
Triangle Park, NC 27111.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  S. P. Levick, D. C. Loch, S. M. Taylor, and J. S. Janicki Arachidonic Acid Metabolism as a Potential Mediator of Cardiac Fibrosis Associated with Inflammation J. Immunol., January 15, 2007; 178(2): 641 - 646. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Monjazeb, K. P. High, A. Connoy, L. S. Hart, C. Koumenis, and F. H. Chilton Arachidonic acid-induced gene expression in colon cancer cells Carcinogenesis, October 1, 2006; 27(10): 1950 - 1960. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. N. Fonteh, C. R. Marion, B. J. Barham, M. B. Edens, G.-i. Atsumi, J. M. Samet, K. P. High, and F. H. Chilton Enhancement of Mast Cell Survival: A Novel Function of Some Secretory Phospholipase A2 Isotypes J. Immunol., October 15, 2001; 167(8): 4161 - 4171. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. W. Anthonsen, S. Andersen, A. Solhaug, and B. Johansen Atypical lambda /iota PKC Conveys 5-Lipoxygenase/Leukotriene B4-mediated Cross-talk between Phospholipase A2s Regulating NF-kappa B Activation in Response to Tumor Necrosis Factor-alpha and Interleukin-1beta J. Biol. Chem., September 14, 2001; 276(38): 35344 - 35351. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |