![]()
|
|
||||||||
J. Biol. Chem., Vol. 275, Issue 22, 16579-16589, June 2, 2000
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Department of Medicine, Mass Spectrometry Facility,
Division of Endocrinology, Diabetes, and Metabolism, Washington
University School of Medicine, St. Louis, Missouri 63110
Upon differentiation, U937 promonocytic cells
gain the ability to release a large fraction of arachidonate esterified
in phospholipids when stimulated, but the mechanism is unclear. U937
cells express group IV phospholipase A2
(cPLA2), but neither its level nor its phosphorylation
state increases upon differentiation. A group VI PLA2
(iPLA2) that is sensitive to a bromoenol lactone inhibitor catalyzes arachidonate hydrolysis from phospholipids in some cells and
facilitates arachidonate incorporation into glycerophosphocholine (GPC)
lipids in others, but it is not known whether U937 cells express
iPLA2. We confirm that ionophore A23187 induces substantial [3H]arachidonate release from differentiated but not
control U937 cells, and electrospray ionization mass spectrometric
(ESI/MS) analyses indicate that differentiated cells contain a higher
proportion of arachidonate-containing GPC species than control cells.
U937 cells express iPLA2 mRNA and activity, but
iPLA2 inhibition impairs neither
[3H]arachidonate incorporation into nor release from U937
cells. Experiments with phosphatidate phosphohydrolase (PAPH) and
phospholipase D (PLD) inhibitors coupled with ESI/MS analyses of
PLD-PAPH products indicate that differentiated cells gain the ability
to produce diacylglycerol (DAG) via PLD-PAPH. DAG promotes arachidonate
release by a mechanism that does not require DAG hydrolysis, is largely independent of protein kinase C, and requires cPLA2
activity. This may reflect DAG effects on cPLA2 substrate state.
Electrospray Ionization/Mass Spectrometric Analyses of Human
Promonocytic U937 Cell Glycerolipids and Evidence That Differentiation
Is Associated with Membrane Lipid Composition Changes That Facilitate
Phospholipase A2 Activation*
*
This work was supported by United States Public Health
Service Grants P01-HL57278, P41-RR00954, P60-DK20579, and R37-DK34388 and the Juvenile Diabetes Foundation Grant 996003).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 correspondence should be addressed: Box 8127, Washington
University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110. Tel.: 314-362-8190; Fax: 314-362-8188.
This article has been cited by other articles:
![]() |
S. Bao, Y. Li, X. Lei, M. Wohltmann, W. Jin, A. Bohrer, C. F. Semenkovich, S. Ramanadham, I. Tabas, and J. Turk Attenuated Free Cholesterol Loading-induced Apoptosis but Preserved Phospholipid Composition of Peritoneal Macrophages from Mice That Do Not Express Group VIA Phospholipase A2 J. Biol. Chem., September 14, 2007; 282(37): 27100 - 27114. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. A. Jacobson, C. R. Weber, S. Bao, J. Turk, and L. H. Philipson Modulation of the Pancreatic Islet beta-Cell-delayed Rectifier Potassium Channel Kv2.1 by the Polyunsaturated Fatty Acid Arachidonate J. Biol. Chem., March 9, 2007; 282(10): 7442 - 7449. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Song, X. Zhang, C. Zhao, N. T. Ang, and Z. A. Ma Inhibition of Ca2+-Independent Phospholipase A2 Results in Insufficient Insulin Secretion and Impaired Glucose Tolerance Mol. Endocrinol., February 1, 2005; 19(2): 504 - 515. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Perez, R. Melero, M. A. Balboa, and J. Balsinde Role of Group VIA Calcium-independent Phospholipase A2 in Arachidonic Acid Release, Phospholipid Fatty Acid Incorporation, and Apoptosis in U937 Cells Responding to Hydrogen Peroxide J. Biol. Chem., September 24, 2004; 279(39): 40385 - 40391. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. Balboa, R. Perez, and J. Balsinde Amplification Mechanisms of Inflammation: Paracrine Stimulation of Arachidonic Acid Mobilization by Secreted Phospholipase A2 Is Regulated by Cytosolic Phospholipase A2-Derived Hydroperoxyeicosatetraenoic Acid J. Immunol., July 15, 2003; 171(2): 989 - 994. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. A. Balboa and J. Balsinde Involvement of Calcium-independent Phospholipase A2 in Hydrogen Peroxide-induced Accumulation of Free Fatty Acids in Human U937 Cells J. Biol. Chem., October 18, 2002; 277(43): 40384 - 40389. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Welti, W. Li, M. Li, Y. Sang, H. Biesiada, H.-E Zhou, C. B. Rajashekar, T. D. Williams, and X. Wang Profiling Membrane Lipids in Plant Stress Responses. ROLE OF PHOSPHOLIPASE Dalpha IN FREEZING-INDUCED LIPID CHANGES IN ARABIDOPSIS J. Biol. Chem., August 23, 2002; 277(35): 31994 - 32002. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Koivusalo, P. Haimi, L. Heikinheimo, R. Kostiainen, and P. Somerharju Quantitative determination of phospholipid compositions by ESI-MS: effects of acyl chain length, unsaturation, and lipid concentration on instrument response J. Lipid Res., April 1, 2001; 42(4): 663 - 672. [Abstract] [Full Text] |
||||
![]() |
Z. Ma, S. Ramanadham, M. Wohltmann, A. Bohrer, F.-F. Hsu, and J. Turk Studies of Insulin Secretory Responses and of Arachidonic Acid Incorporation into Phospholipids of Stably Transfected Insulinoma Cells That Overexpress Group VIA Phospholipase A2 (iPLA2beta ) Indicate a Signaling Rather Than a Housekeeping Role for iPLA2beta J. Biol. Chem., April 13, 2001; 276(16): 13198 - 13208. [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 |