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

Abstract

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.

Replication Potential of Cells via the Protein Kinase C-MAPK pathway: Application of a Mathematical Model

“…factor (GF) in equation (1) in agreement with previously published data produced by Buckley et al (1991). Figure 5 illustrates the fit of the model simulations for fos and jun mRNA levels to their respective data.…”

Regulation of Blood Vessels by Prolactin and Vasoinhibins

“…Liver growth is angiogenesis-dependent and coincides with the hyperprolactinemia ocurring during pregnancy and lactation, cirrhosis [68], and after partial hepatectomy [69]. Absence of the PRL receptor confers reduced liver mass, and elevating systemic PRL promotes growth and neovascularization of the normal and regenerating adult liver [38].…”

Screening for candidate hepatic growth factors by selective portal infusion after canine Eck's fistula

“…TGF-a is a stronger mitogen than EGF for hepatocytes in vitro (23), and in many other functions besides hepatocyte replication it is a stronger affector (24). Other putative stimulators that had little or no effect in Eck's fistula preparation included the hormones prolactin (25), angiotensin II (26), vasopressin (7), norepinephrine (6,27), estradiol (28) and glucagon (29).…”