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Molecular Pharmacology, Vol 20, 609-613, Copyright © 1981 by the American Society for Pharmacology and Experimental Therapeutics

Stimulation of Human Placental Lactogen Release by Arachidonic Acid

S. HANDWERGER 1, J. BARRETT 1, S. BARRY 1, E. MARKOFF 1, P. ZEITLER 1, B. CWIKEL 1, and M. SIEGEL 1

1 Departments of Pediatrics and Physiology, Duke University Medical Center, Durham, North Carolina, 27710, Department of Hormone Research, Weizmann Institute of Science, Rehovot, Israel and Wellcome Research Laboratories, Research Triangle Park, North Carolina, 27709

Arachidonic acid at concentrations between 20 and 300 µM stimulated human placental lactogen (hPL) release from placental explants in a dose-dependent manner (R = 0.90, p < 0.001). Explants incubated for 2 hr in medium containing 20 µM arachidonic acid released 97.0 ± 12.1% (mean ± SE, p < 0.05) more hPL than did control explants, whereas explants incubated in medium containing 300 µM arachidonic acid released 514.2 ± 18.7% (p < 0.001) more hPL. Phospholipase A2 (0.11 unit/ml), which cleaves arachidonic acid from the 2-acyl position of phospholipids, stimulated hPL release by 2272.6 ± 219.6% (p < 0.001). Neither arachidonic acid nor phospholipase A2 affected the release of human chorionic gonadotropin, lactic dehydrogenase, or alkaline phosphatase, and arachidonic acid had no effect on the release of trichloroacetic acid-precipitable 35S-labeled proteins. The fatty acid precursors of arachidonic acid—linoleic, ggr-linolenic, and dihomo-ggr-linolenic acids—also stimulated hPL release, but 11,14,17-icosatrienoic, oleic, and palmitic acids had no statistically significant effects. The cyclo-oxygenase inhibitors indomethacin (14 µM) and flufenamic acid (18 µM) had no effects on either the basal release of hPL or the stimulatory affect of arachidonic acid. In addition, the cyclo-oxygenase products prostaglandins E1, E2, and F2agr had no effects on hPL release. The lipoxygenase inhibitors 5,8,11,14-icosatetraynoic acid (82 µM) and BW755C (20 µM) had no effects on basal hPL release but potentiated the stimulatory effect of arachidonic acid. These results suggest that arachidonic acid may stimulate hPL release via a non-cyclo-oxygenase, non-lipoxygenase pathway.

Note:
ACKNOWLEDGMENTS We thank Drs. P. Michael Conn and R. M. Bell for their suggestions, and G. M. Kerr for typing the manuscript.

Submitted on April 3, 1981
Accepted on July 27, 1981






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