Arachidonic acid release by cPLA2 may be causally related to NO-induced apoptosis in vascular smooth muscle cells

2002 ◽  
Vol 191 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Cyril M. Pilane ◽  
Edward F. LaBelle
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
Induced Apoptosis

scholarly journals Angiotensin II stimulates phosphorylation of high-molecular-mass cytosolic phospholipase A2 in vascular smooth-muscle cells

1994 ◽  
Vol 299 (1) ◽  
pp. 197-201 ◽  
Author(s):  
G N Rao ◽  
B Lassègue ◽  
R W Alexander ◽  
K K Griendling
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Time Dependent ◽  
Arachidonic Acid Release ◽  
Acid Release

Phospholipase A2 (PLA2) may be one of the major components involved in cell signalling and proliferation, as suggested by recent studies. In this paper we show that the potent vasoconstrictor and hypertrophic agent angiotensin II (AngII) activates cytosolic PLA2 (cPLA2) in vascular smooth-muscle cells. AngII induced a rapid time-dependent release of [3H]arachidonic acid from prelabelled cells that was inhibited by mepacrine, a PLA2 inhibitor. AngII treatment of intact cells also activated a cPLA2, as measured in cell-free extracts by the release of radiolabelled arachidonic acid from exogenously added 1-stearoyl-2-[1-14C]arachidonoyl phosphatidylcholine. This AngII-stimulated cPLA2 activity was also significantly inhibited by mepacrine. AngII induced a rapid and time-dependent increase in cPLA2 phosphorylation. Protein kinase C (PKC) depletion inhibited both AngII-induced [3H]arachidonic acid release and cPLA2 phosphorylation. Together, these results suggest strongly that (1) AngII phosphorylates and activates cPLA2 in a PKC-dependent manner, and that (2) cPLA2 mediates the AngII-induced [3H]arachidonic acid release in vascular smooth-muscle cells.

Endothelin and PDGF enhance arachidonic acid release and DNA synthesis in vascular smooth muscle cells

1996 ◽  
Vol 270 (6) ◽  
pp. C1642-C1646 ◽  
Author(s):  
C. E. Irons ◽  
M. A. Flynn ◽  
L. M. Mok ◽  
E. E. Reynolds
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Thymidine Incorporation ◽  
Cell Number ◽  
Arachidonic Acid Release ◽  
Acid Release

Intracellular signaling mechanisms affected by endothelin (ET), a hypertrophic agonist, and platelet-derived growth factor (PDGF)-BB, a proliferative agonist, in vascular smooth muscle cells were examined. PDGF-BB was a potent mitogen compared with untreated cultures, stimulating both [3H]thymidine incorporation and cell number. In contrast, ET was a poor mitogen, enhancing [3H]thymidine incorporation but not cell number. Simultaneous ET and PDGF-BB treatment was significantly more effective than either agonist alone at stimulating both [3H]thymidine uptake and cell number. Although either ET or PDGF-BB alone stimulated arachidonic acid release, phosphoinositide hydrolysis, protein kinase C activation, PDGF receptor phosphorylation, and mitogen-activated protein kinase activity, of these effectors, only arachidonic acid release was further enhanced by simultaneous ET and PDGF-BB treatment. These results link proliferative and hypertrophic signal transduction pathways in these cells and suggest that arachidonic acid or its metabolites mediate the observed effects of ET on PDGF-BB-stimulated vascular smooth muscle cell proliferation.

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