Partial hepatectomy (HPX), which proliferatively activates the remaining liver cells, triggered two transient prereplicative surges in the total activities of cytoplasmic types I and II cyclic AMP-dependent protein kinase holoenzymes, and of nuclear catalytic subunits from cyclic AMP-dependent protein kinases. It also induced a transient prereplicative increase in the activities of a nuclear Ca2+-calmodulin-stimulable, protamine-phosphorylating protein kinase, and a nuclear poly(L-lysine)-phosphorylating, 105 kDa protein kinase. Thyroparathyroidectomy (TPTX) delayed and reduced the first surge and completely eliminated the second surge of both of the cytoplasmic cyclic AMP-dependent protein kinases, reduced the rises in the activity of nuclear catalytic subunits, and completely eliminated the surge of the Ca2+-calmodulin-stimulable protein kinase, but did not affect the surge of the nuclear 105 kDa protein kinase. The impairment of the responses of the two cyclic AMP-dependent protein kinases to HPX in TPTX rats was not accompanied by a rise in the level of heat-stable inhibitor of cyclic AMP-dependent protein kinase activity. One intraperitoneal injection of 1,25-dihydroxyvitamin D1 into TPTX rats immediately after HPX completely restored the post-HPX surges in the activity of type I cyclic AMP-dependent protein kinase, but the hormone, even in high doses, had little or not effect on the type II isoenzyme or the nuclear Ca2+-calmodulin-stimulable, protamine-phosphorylating enzyme.
A single intraperitoneal injection of a commercia1 preparation ofka1likrein (3 or 5 units/lOO gm) stimulated the mitotic aotivity of cells in the thymus gland and the bone marrow of rats. This'effect was observed three to six hours after injeotion as an increase in the mitotic index and the accumulation of ceRs in the metaphase stage of mitosis by the mitotic blocking agent, colcemid Kallikrein did not affect the mitotic aotivity of isolated thymic lymphocytes. The release of mitogenically-active kinins is proposed as the means by which kallikrein enhances ceR proliferation in lIil'O.Horn Metab. Res. 3: 279-284 (1971) K e y -W 0 r d s: Kallikrein -Mitotic Stimulotion -Thy· mus -Bone Ma"ow
Growth hormone (GH) considerably increases the flow of cells into mitosis in rat thymic lymphocyte (thymocyte) populations maintained in vitro. This calcium-dependent, cyclic-AMP-mediated mitogenic action of GH is due to the rapid (within 60 minutes) stimulation of the initiation of deoxyribonudeic acid (DNA) synthesis in apart of the thymocyte population which is poised, or blocked, at the threshold of the DNA-synthetic (S) phase of the cell cycle. A possible mechanism by wh ich GH, through the agency of cyclic AMP, could promote the initiation of DNA synthesis is discussed.
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