PGE1 not PGF2 alpha reverses the anti-actin antibody stimulation of protein phosphorylation and DNA synthesis in L cells.
The effects of prostaglandins E1 and F2 alpha upon the anti-actin antibody-induced stimulation of DNA synthesis and protein phosphorylation were studied in L cells. This system was previously shown by us to exhibit a rapid turnover of arachidonic acid in phospholipids which was inhibited by non-toxic concentrations of indomethacin, suggesting participation of cyclooxygenase-derived prostaglandins (Lipids 19:239, 1984). Prostaglandin E1 in a dose dependent manner selectively inhibited both protein phosphorylation and DNA synthesis in anti-actin antibody-stimulated cells. Prostaglandin F2 alpha was without effect. Indomethacin also produced a dose related inhibition of the antibody stimulation of protein phosphorylation and DNA synthesis. We conclude that prostaglandins, possibly derived from liberated arachidonic acid, play an important regulatory role in the stimulatory signal conveyed to L cells by perturbing antibody ligands.
D000199:Actins / Q000276:immunology / Q000378:metabolism*; D000527:Alprostadil; D000818:Animals; D000906:Antibodies; D000936:Antigen-Antibody Complex; D004261:DNA Replication / Q000187:drug effects*; D015237:Dinoprost; D007700:Kinetics; D007739:L Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D010766:Phosphorylation; D011458:Prostaglandins E / Q000494:pharmacology*; D011460:Prostaglandins F / Q000494:pharmacology*; D011506:Proteins / Q000378:metabolism*
D000199:Actins; D000906:Antibodies; D000936:Antigen-Antibody Complex; D011458:Prostaglandins E; D011460:Prostaglandins F; D011506:Proteins; D015237:Dinoprost; D000527:Alprostadil