Document Detail

Ca(2+)-independent phospholipase A2 is required for alpha2-adrenergic-induced preadipocyte spreading.
MedLine Citation:
PMID:  10558911     Owner:  NLM     Status:  MEDLINE    
In the present study, we studied the involvement of A2 phospholipases (PLA2) in alpha2-adrenergic receptor-control of preadipocyte actin cytoskeleton. For that, various PLA2 inhibitors were tested on the ability of the selective alpha2-adrenergic agonist UK14304 to induce the spreading in alpha2AF2 preadipocytes. We observed that, whereas several Ca(2+)-dependent PLA2 blockers were ineffective, the Ca(2+)-independent phospholipase A2 (iPLA2) inhibitor, broenolactone (BEL), specifically blocked alpha2-adrenergic-dependent preadipocyte spreading without affecting the spreading activity of lysophosphatidic acid (LPA) or serum. BEL inhibition was completely restored by lysophosphatidic acid, but not by arachidonic acid or other fatty acids. The presence of the lysophospholipase (phospholipase B) suppressed the effect of LPA on preadipocyte spreading, but had no influence on alpha2-adrenergic-induced spreading. Thus, the extracellular production of LPA or fatty acids is not involved in iPLA2-dependent preadipocyte spreading. iPLA2 protein was found in preadipocytes but, conversely to cPLA2, did not exhibit any modification of its electrophoretic mobility after alpha2-adrenergic stimulation. We concluded that iPLA2 is involved in alpha2-adrenergic control of preadipocyte actin cytoskeleton.
C Pagès; A Rey; M Lafontan; P Valet; J S Saulnier-Blache
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  265     ISSN:  0006-291X     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  1999 Nov 
Date Detail:
Created Date:  1999-12-20     Completed Date:  1999-12-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  572-6     Citation Subset:  IM    
Copyright Information:
Copyright 1999 Academic Press.
Institut Louis Bugnard, Université Paul Sabatier, CHU Rangueil, Batiment L3, Toulouse cedex 04, 31403, France.
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MeSH Terms
3T3 Cells
Actins / metabolism
Adipocytes / cytology,  drug effects,  metabolism*
Adrenergic alpha-Agonists / pharmacology
Base Sequence
Calcium / metabolism
Cell Adhesion / drug effects,  physiology
Cytoskeleton / metabolism
DNA Primers / genetics
Lysophospholipids / pharmacology
Naphthalenes / pharmacology
Phospholipases A / antagonists & inhibitors,  genetics,  metabolism*
Phospholipases A2
Pyrones / pharmacology
Quinoxalines / pharmacology
RNA, Messenger / genetics,  metabolism
Receptors, Adrenergic, alpha-2 / metabolism*
Stem Cells / cytology,  drug effects,  metabolism
Reg. No./Substance:
0/Actins; 0/Adrenergic alpha-Agonists; 0/DNA Primers; 0/Lysophospholipids; 0/Naphthalenes; 0/Pyrones; 0/Quinoxalines; 0/RNA, Messenger; 0/Receptors, Adrenergic, alpha-2; 59803-98-4/brimonidine; 7440-70-2/Calcium; 88070-98-8/6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-one; EC 3.1.1.-/Phospholipases A; EC A2

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