important mitogcnic action of parathyroid hormone, it is proposed that thyrocalcitonin (calcitonin) may bc a general regulator of cyclic AMP-controlled cell proliferation in vivo.
During the fust 10 min after exposure of rat thymic Iymphocytes (thymocytes) to a high concentration (5.0 /.I8/m!) of prostagiandin EI (PGE I ) in medium without added calcium, there is a 67-fold rise in the ceUular cyclic AMP content which causes strong stimulations of deoxyribunucleic acid (DNA) synthesis and cell proliferation. On the other hand, in the presence of 1.0 mM calcium, PGE I causes a similar (68-fold) rise in the cellular cyclic AMP content and a strong stimulation of DNA synthesis, but the stimulated cells do not enter mitosis. Thus, calcium selectively inhibits the cyclic AMP-induced mitogenic process.The calcium-sensitive phase of the mitogenic reaction is normally completed by only 2.5 min after exposure to PGE I; addition of calcium to the extracellular fluid at, or after, this time does not inhibit the flow of stimulated cells into mitosis which begins between 3 and 4 hr later. Finally, calcium must inhibit the operation, but not the cyclic AMPmediated activation, of the mitogenic system since the inhibition can be fully relieved by removal of calcium at least 4 br after exposure to PGE I.
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