Effects of omega-3 fatty acids on vascular smooth muscle cells: Reduction in arachidonic acid incorporation into inositol phospholipids

Lipids ◽  
1989 ◽  
Vol 24 (7) ◽  
pp. 594-602 ◽  
Author(s):  
Nagender R. Yerram ◽  
Arthur A. Spector
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Acid Incorporation ◽  
Inositol Phospholipids

scholarly journals Omega-3 Fatty Acids Inhibit Thrombin Formation In Vascular Smooth Muscle Cells

2019 ◽  
Vol 287 ◽  
pp. e27-e28
Author(s):  
N.T. Skenteris ◽  
J. Pirault ◽  
M. Didelot ◽  
P. Lacolley ◽  
V. Regnault ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Thrombin Formation

scholarly journals Omega-3 Fatty Acid-Derived Resolvin D2 Regulates Human Placental Vascular Smooth Muscle and Extravillous Trophoblast Activities

2019 ◽  
Vol 20 (18) ◽  
pp. 4402 ◽  
Author(s):  
Arzu Ulu ◽  
Prakash K. Sahoo ◽  
Ana G. Yuil-Valdes ◽  
Maheswari Mukherjee ◽  
Matthew Van Ormer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Placental Tissue ◽  
Cell Types ◽  
Extravillous Trophoblast ◽  
Protective Effects ◽  
Omega 3 Fatty Acids ◽  
Omega 3

Omega-3 fatty acids are important to pregnancy and neonatal development and health. One mechanism by which omega-3 fatty acids exert their protective effects is through serving as substrates for the generation of specialized pro-resolving lipid mediators (SPM) that potently limit and resolve inflammatory processes. We recently identified that SPM levels are increased in maternal blood at delivery as compared to umbilical cord blood, suggesting the placenta as a potential site of action for maternal SPM. To explore this hypothesis, we obtained human placental samples and stained for the SPM resolvin D2 (RvD2) receptor GPR18 via immunohistochemistry. In so doing, we identified GPR18 expression in placental vascular smooth muscle and extravillous trophoblasts of the placental tissues. Using in vitro culturing, we confirmed expression of GPR18 in these cell types and further identified that stimulation with RvD2 led to significantly altered responsiveness (cytoskeletal changes and pro-inflammatory cytokine production) to lipopolysaccharide inflammatory stimulation in human umbilical artery smooth muscle cells and placental trophoblasts. Taken together, these findings establish a role for SPM actions in human placental tissue.

Free Fatty Acids Induce Autophagy and LOX-1 Upregulation in Cultured Aortic Vascular Smooth Muscle Cells

2017 ◽  
Vol 118 (5) ◽  
pp. 1249-1261 ◽  
Author(s):  
Cheng-I Cheng ◽  
Yueh-Hong Lee ◽  
Po-Han Chen ◽  
Yu-Chun Lin ◽  
Ming-Huei Chou ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Free Fatty Acids ◽  
Vascular Smooth Muscle Cells ◽  
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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