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Evidence that Phorbol Diester-Sensitive Protein Kinase C(s) May not Be Directly Involved in Secretagogue-Stimulated Prolactin Release and Arachidonate Liberation^*

Departments of Internal Medicine
Neurology, and the Center for Cancer Research, University of Virginia Health Sciences Center Charlottesville, Virginia 22908

Address requests for reprints to: Dr. Robert M. MacLeod, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908.

Abstract

This report presents findings pertaining to the role of protein kinase-Cs in the release of PRL and liberation of arachidonate from PRL-secreting cells. In our experiments, protein kinase-C activators increased PRL release and arachidonate liberation from anterior pituitary cells and from the PRL-secreting cell line MMQ. In cells depleted of pituitary protein kinase-Cs by chronic exposure to protein kinase-C activators, such as phorbol dibutyrate or 4β-phorbol 12β-myristate 13acetate, TRH, angiotensin-II, and neurotensin each increased PRL release and [³H]arachidonate liberation in a normal manner. In addition, the PRL-releasing activities of protein kinase-C activators and those of TRH appeared to be synergistic, an unexpected effect if these substances were functioning through the same intracellular pathways. It, therefore, appears that phorbol diester-sensitive protein kinase-Cs may not be involved in the increased secretion of PRL or liberation of arachidonate that is caused by TRH, angiotensin-II, or neurotensin.

Footnotes

^* This work was supported by NIH Grants CA-07535-24 (to R.M.M.) and CA-38228 (to I.S.L.) from the NCI.

Received March 27, 1989.