Increase of phosphoinositide hydrolysis and diacylglycerol production by PAF in isolated rat liver nuclei.
When isolated rat liver nuclei were treated with platelet-activating factor (PAF), a rapid increase in the mass of diacylglycerol (DAG) occurred. This effect was dose- and time-dependent. The maximum effect was observed after 1 min of 10(-7) M PAF treatment. A concomitant decrease of polyphosphoinositides and phosphatidic acid (PA) levels was observed. PAF-induced DAG accumulation was inhibited by the treatment with WEB 2086 or PCA-4248, specific PAF-receptor antagonists. This result may suggest that PAF exerts its action in the nucleus through specific nuclear PAF binding sites. The findings described herein are due to the activation of phospholipase C, as the results from experiments using U73122, a phospholipase C inhibitor, indicate. These are the first data on the action of
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in isolated nuclei, and they suggest a modulation by PAF of intranuclear signal transduction within the nucleus, possibly by specific PAF receptors.
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Martín
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D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002467:Cell Nucleus / Q000187:drug effects* / Q000378:metabolism; D004075:Diglycerides / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism*; D006868:Hydrolysis; D008297:Male; D010716:Phosphatidylinositols / Q000378:metabolism*; D010972:Platelet Activating Factor / Q000494:pharmacology*; D010980:Platelet Membrane Glycoproteins / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D013997:Time Factors; D010738:Type C Phospholipases / Q000378:metabolism
D004075:Diglycerides; D010716:Phosphatidylinositols; D010972:Platelet Activating Factor; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D000255:Adenosine Triphosphate; D010738:Type C Phospholipases