The effects of thyroparathyroidectomy and 1,25 dihydroxyvitamin D3 on changes in the activities of some cytoplasmic and nuclear protein kinases during liver regeneration

• Published in: Journal of cellular physiology Vol. 115; no. 3; p. 297
• Main Authors: Sikorska, M, Whitefield, J F, Rixon, R H
• Format: Journal Article
• Language: English
• Published: United States 01-06-1983
• Subjects: Animals; Calcitriol - pharmacology; Calcium - pharmacology; Calmodulin - pharmacology; Cell Nucleus - enzymology; Cytoplasm - enzymology; Hepatectomy; Liver - enzymology; Liver Regeneration; Male; Parathyroid Glands - surgery; Protein Kinases - metabolism; Rats; Rats, Inbred Strains; Thyroidectomy
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041150313

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.