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Research Article Free access | 10.1172/JCI117539

Proliferation-dependent changes in release of arachidonic acid from endothelial cells.

R E Whatley, K Satoh, G A Zimmerman, T M McIntyre, and S M Prescott

Veterans Affairs Medical Center, Salt Lake City, Utah.

Find articles by Whatley, R. in: PubMed | Google Scholar

Veterans Affairs Medical Center, Salt Lake City, Utah.

Find articles by Satoh, K. in: PubMed | Google Scholar

Veterans Affairs Medical Center, Salt Lake City, Utah.

Find articles by Zimmerman, G. in: PubMed | Google Scholar

Veterans Affairs Medical Center, Salt Lake City, Utah.

Find articles by McIntyre, T. in: PubMed | Google Scholar

Veterans Affairs Medical Center, Salt Lake City, Utah.

Find articles by Prescott, S. in: PubMed | Google Scholar

Published November 1, 1994 - More info

Published in Volume 94, Issue 5 on November 1, 1994
J Clin Invest. 1994;94(5):1889–1900. https://doi.org/10.1172/JCI117539.
© 1994 The American Society for Clinical Investigation
Published November 1, 1994 - Version history
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Abstract

Stimulation of endothelial cells resulted in release of arachidonic acid from phospholipids. The magnitude of this response decreased as the cells became confluent and the change coincided with a decrease in the percentage of cells in growth phases (G2+M); this was not a consequence of time in culture or a factor in the growth medium. Preconfluent cells released approximately 30% of arachidonic acid; confluent cells released only 6%. The decreasing release of arachidonic acid was demonstrated using metabolic labeling, mass measurements of arachidonic acid, and measurement of PGI2. The decrease was not due to a changing pool of arachidonic acid, and mass measurements showed no depletion of arachidonic acid. Release from each phospholipid and from each phospholipid class decreased with confluence. Conversion of confluent cells to the proliferative phenotype by mechanical wounding of the monolayer caused increased release of arachidonic acid. Potential mechanisms for these changes were investigated using assays of phospholipase activity. Phospholipase A2 activity changed in concert with the alteration in release, a consequence of changes in phosphorylation of the enzyme. The increased release of arachidonic acid from preconfluent, actively dividing cells may have important physiologic implications and may help elucidate mechanisms regulating release of arachidonic acid.

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