scholarly journals Integrin-dependent homotypic adhesion of neutrophils. Arachidonic acid activates Raf-1/Mek/Erk via a 5-lipoxygenase- dependent pathway.

1998 ◽  
Vol 102 (1) ◽  
pp. 165-175 ◽  
Author(s):  
C Capodici ◽  
M H Pillinger ◽  
G Han ◽  
M R Philips ◽  
G Weissmann
Keyword(s):  
Arachidonic Acid ◽  
Dependent Pathway ◽  
Homotypic Adhesion

Arachidonic acid supplementation enhances in vitro skeletal muscle cell growth via a COX-2-dependent pathway

2013 ◽  
Vol 304 (1) ◽  
pp. C56-C67 ◽  
Author(s):  
James F. Markworth ◽  
David Cameron-Smith
Keyword(s):  
Skeletal Muscle ◽  
Arachidonic Acid ◽  
Cell Growth ◽  
Muscle Cell ◽  
Myogenic Differentiation ◽  
Skeletal Muscle Cell ◽  
Diverse Range ◽  
Cox 2 ◽  
Dependent Pathway

Arachidonic acid (AA) is the metabolic precursor to a diverse range of downstream bioactive lipid mediators. A positive or negative influence of individual eicosanoid species [e.g., prostaglandins (PGs), leukotrienes, and hydroxyeicosatetraenoic acids] has been implicated in skeletal muscle cell growth and development. The collective role of AA-derived metabolites in physiological states of skeletal muscle growth/atrophy remains unclear. The present study aimed to determine the direct effect of free AA supplementation and subsequent eicosanoid biosynthesis on skeletal myocyte growth in vitro . C2C12 (mouse) skeletal myocytes induced to differentiate with supplemental AA exhibited dose-dependent increases in the size, myonuclear content, and protein accretion of developing myotubes, independent of changes in cell density or the rate/extent of myogenic differentiation. Nonselective (indomethacin) or cyclooxygenase 2 (COX-2)-selective (NS-398) nonsteroidal anti-inflammatory drugs blunted basal myogenesis, an effect that was amplified in the presence of supplemental free AA substrate. The stimulatory effects of AA persisted in preexisting myotubes via a COX-2-dependent (NS-389-sensitive) pathway, specifically implying dependency on downstream PG biosynthesis. AA-stimulated growth was associated with markedly increased secretion of PGF2α and PGE2; however, incubation of myocytes with PG-rich conditioned medium failed to mimic the effects of direct AA supplementation. In vitro AA supplementation stimulates PG release and skeletal muscle cell hypertrophy via a COX-2-dependent pathway.

Oleic acid promotes migration on MDA-MB-231 breast cancer cells through an arachidonic acid-dependent pathway

2010 ◽  
Vol 42 (2) ◽  
pp. 306-317 ◽  
Author(s):  
Napoleon Navarro-Tito ◽  
Adriana Soto-Guzman ◽  
Luis Castro-Sanchez ◽  
Raul Martinez-Orozco ◽  
Eduardo Perez Salazar
Keyword(s):  
Breast Cancer ◽  
Arachidonic Acid ◽  
Oleic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Dependent Pathway

Angiotensin II activates Akt/protein kinase B by an arachidonic acid/redox‐dependent pathway and independent of phosphoinositide 3‐kinase

2001 ◽  
Vol 15 (11) ◽  
pp. 1909-1920 ◽  
Author(s):  
Yves Gorin ◽  
Nam‐Ho Kim ◽  
Denis Feliers ◽  
Basant Bhandari ◽  
Goutam Ghosh Choudhury ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Ii ◽  
Protein Kinase ◽  
Protein Kinase B ◽  
Phosphoinositide 3 Kinase ◽  
Dependent Pathway

scholarly journals Arachidonic acid inhibits the production of angiotensin-converting enzyme in human primary adipocytes via a NF-κB-dependent pathway

2020 ◽  
Vol 8 (24) ◽  
pp. 1652-1652
Author(s):  
Li Xu ◽  
Rita Schüler ◽  
Chenchen Xu ◽  
Nicole Seebeck ◽  
Mariya Markova ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Dependent Pathway

Arachidonic Acid-Dependent Pathway Inhibition in Platelets: its Role in Multiple Injury-Induced Coagulopathy and the Potential Mechanisms

Shock ◽  
2020 ◽  
Vol 55 (1) ◽  
pp. 121-127 ◽  
Author(s):  
Yao Tang ◽  
Sunhua Huang ◽  
Wenhao Lin ◽  
Ke Wen ◽  
Zhexuan Lin ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Multiple Injury ◽  
Pathway Inhibition ◽  
Dependent Pathway

Role of 100-kDa cytosolic PLA2 in ACh-induced contraction of cat esophageal circular muscle

1994 ◽  
Vol 267 (3) ◽  
pp. G433-G441 ◽  
Author(s):  
U. D. Sohn ◽  
D. K. Kim ◽  
J. V. Bonventre ◽  
J. Behar ◽  
P. Biancani
Keyword(s):  
Arachidonic Acid ◽  
Circular Muscle ◽  
Nordihydroguaiaretic Acid ◽  
Kinase C ◽  
Acid Release ◽  
Esophageal Sphincter ◽  
Cytosolic Pla2 ◽  
Dependent Pathway ◽  
Esophageal Contraction

We have shown that acetylcholine (ACh)-induced contraction of esophageal circular muscle cells is mediated by activation of protein kinase C (PKC). We now examine the role of phospholipase A2 (PLA2). ACh increases [3H]arachidonic acid release in esophageal but not in lower esophageal sphincter (LES) muscle. In addition, ACh-induced contraction of esophageal but not of LES cells was reduced by the PLA2 antagonist dimethyleicosadienoic acid and by antiserum to a 100-kDa cytosolic PLA2 (cPLA2). These data suggest that the 100-kDa cPLA2 plays a role in ACh-induced contraction of esophageal but not of LES muscle. In esophageal cells, arachidonic acid produced by PLA2 caused little contraction by itself but potentiated contraction induced by the PKC agonist diacylglycerol (DAG). The free fatty acids linoleic acid and linolenic acid also potentiated DAG-induced contraction. Indomethacin and nordihydroguaiaretic acid had no effect on arachidonic acid-induced potentiation of DAG. The potentiation of DAG-induced contraction by arachidonic acid was inhibited by the PKC inhibitor H-7, but it was not affected by the calmodulin inhibitor CGS-9343B. We conclude that a 100-kDa cPLA2 participates in ACh-induced esophageal contraction by producing arachidonic acid and potentiating DAG-induced activation of a PKC-dependent pathway.

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