Prolactin-provoked alterations of cytosolic, membrane, and nuclear protein kinase C following partial hepatectomy

Arthur R. Buckley, Paul D. Crowe, Patricia A. Bauman, Leigh A Neumayer, Hugh E. Laird, Diane Haddock Russell, Charles W. Putnam

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


The adenohypophyseal polypeptide hormone prolactin is a potent liver mitogen, stimulating cell cycle progression, an effect that appears coupled to increasing protein kinase C activity in membrane and nuclear fractions. Here, we examine whether hepatocyte proliferation, stimulated by partial hepatectomy, is associated with altered serum prolactin or protein kinase C activation. Within 5-15 min of liver resection, serum prolactin concentrations elevate significantly. Protein kinase C activity in hepatic cytosol decreases significantly, and membrane and nuclear PKC activity increase by 30 min. Hypophysectomy prior to partial hepatectomy abrogates any effect of liver resection on protein kinase C activation in the hepatic remnant. Based upon these data, it is suggested that the rapid increase in serum prolactin seen after partial hepatectomy may be linked to protein kinase C activation, which in turn stimulates the hepatic proliferative response that is essential for hepatic regeneration.

Original languageEnglish (US)
Pages (from-to)1313-1319
Number of pages7
JournalDigestive diseases and sciences
Issue number9
StatePublished - Sep 1991


  • hypophysectomy
  • liver regeneration
  • nucleus
  • prolactin
  • protein kinase C

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology


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