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Research Article Free access | 10.1172/JCI115771

Differential expression of guanine nucleotide-binding proteins enhances cAMP synthesis in regenerating rat liver.

A M Diehl, S Q Yang, D Wolfgang, and G Wand

Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21205.

Find articles by Diehl, A. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21205.

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

Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21205.

Find articles by Wolfgang, D. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21205.

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

Published June 1, 1992 - More info

Published in Volume 89, Issue 6 on June 1, 1992
J Clin Invest. 1992;89(6):1706–1712. https://doi.org/10.1172/JCI115771.
© 1992 The American Society for Clinical Investigation
Published June 1, 1992 - Version history
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Abstract

Events leading to cAMP accumulation after partial hepatectomy (PH) and effects of cAMP on hormonal induction of DNA synthesis in hepatocytes were characterized. Hepatic cAMP peaked biphasically post-PH and paralleled changes in adenylyl cyclase activity. Fluctuations in cyclase activity were not explained by variations in glucagon receptor kinetics, but reflected altered G-protein expression. Membrane levels of the stimulatory G-protein, Gs alpha, increased early after PH and were sustained. Levels of the inhibitory G-protein, Gi2 alpha, increased more slowly, peaked later, and quickly fell. Levels of both G-proteins correlated poorly with levels of their mRNAs, suggesting posttranscriptional factors modify their membrane concentrations. When growth factor-induced DNA synthesis was compared in hepatocyte cultures grown with or without agents that increase intracellular cAMP, DNA synthesis was inhibited by sustained high levels of cAMP but was enhanced when high cAMP levels fell. In both regenerating liver and hepatocyte cultures, the expression of a "differentiated" hepatocyte gene, phosphoenolpyruvate carboxykinase, correlated with elevated cAMP levels. These data suggest that the differential expression of G-proteins integrates signals initiated by several growth factors so that the accumulation of cAMP is tightly regulated post-PH. The ensuing variations in cAMP levels modulate both growth and differentiated functions during liver regeneration.

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