ArticleMediators of inflammation2000
Involvement of different protein kinases and phospholipases A2 in phorbol ester (TPA)-induced arachidonic acid liberation in bovine platelets.
Article in Mediators of inflammation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Lysophospholipids Contribute to Oxaliplatin-Induced Acute Peripheral Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Platelet Lipidomic Profiling: Novel Insight into Cytosolic Phospholipase A2α Activity and Its Role in Human Platelet Activation.Biochemistry · 2015Article
- Group VIB calcium-independent phospholipase A2 (iPLA2γ) regulates platelet activation, hemostasis and thrombosis in mice.PloS one · 2014Article
- Effects of the inhibition of cytosolic phospholipase A(2)α in non-small cell lung cancer cells.Journal of cancer research and clinical oncology · 2012Article
- Phospholipase A2-catalyzed hydrolysis of plasmalogen phospholipids in thrombin-stimulated human platelets.Thrombosis research · 2007Article
- Epidermal anti-Inflammatory properties of 5,11,14 20:3: effects on mouse ear edema, PGE2 levels in cultured keratinocytes, and PPAR activation.Lipids in health and disease · 2002Article
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2 authors at 1 institution in 1 country.
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Abstract
The effect of various phospholipase A2 and protein kinase inhibitors on the arachidonic acid liberation in bovine platelets induced by the protein kinase activator 12-O-tetradecanoylphorbol-13-acetate (TPA) was studied. TPA stimulates arachidonic acid release mainly by activating group IV cytosolic PLA2 (cPLA2), since inhibitors of this enzyme markedly inhibited arachidonic acid formation. However, group VI Ca2+-independent PLA2 (iPLA2) seems to contribute to the arachidonic acid liberation too, since the relatively specific iPLA2 inhibitor bromoenol lactone (BEL) decreased arachidonic acid generation in part. The pronounced inhibition of the TPA-induced arachidonic acid release by the protein kinase C (PKC) inhibitors GF 109203X and Ro 31-82220, respectively, and by the p38 MAP kinase inhibitor SB 202190 suggests that the activation of the PLA2s by TPA is mediated via PKC and p38 MAP kinase.
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