Article

Prolactin administration stimulates rat hepatic DNA synthesis.

Department of Pharmacology, University of Arizona College of Medicine, Tucson, AZ 85724, USA; Department of Surgery, University of Arizona College of Medicine, Tucson, AZ 85724, USA; Veterans Administration Medical Center3, Tucson, AZ 85723, USA
Biochemical and Biophysical Research Communications (Impact Factor: 2.28). 09/1986; 138(3):1138-45. DOI: 10.1016/S0006-291X(86)80401-6
Source: PubMed

ABSTRACT Prolactin is an important growth modulatory hormone in fetal and adult tissues. Its administration stimulates enzymatic markers of the G1 phase of cell cycle in rat liver and other tissues. To determine the effects of prolactin administration on hepatic DNA synthesis (S phase), rats received prolactin at 12 hour intervals for 48 hours and DNA synthesis was assessed by [3H]-thymidine incorporation. Prolactin administration stimulated DNA synthesis 2-4 fold above controls in the livers of adult and weanling animals. Increased incorporation of radiolabel was associated with the nucleus of hepatoparenchymal cells. These data support the hypothesis that prolactin may be a physiological regulator of hepatic DNA synthesis. Further, since stress stimulates prolactin secretion, we suggest that prolactin may participate in the hepatic compensatory hyperplasia elicited by the stress associated with partial hepatectomy.

0 Bookmarks
 · 
46 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Mammalian liver is an estrogen-responsive tissue mediated by hepatic estrogen receptors. Although Ueyama et al. (Endocrinology 143:3162-3170, 2002) have reported the presence of aromatase and active production of gastric 17β-estradiol in parietal cells, there are a few studies on gastric 17β-estradiol exploring the relationship between gastro-hepato function and the gastro-pituitary-gonadal axis. The alteration of gastric 17β-estradiol flow into the systemic circulation by portal vein ligation (PVL) or partial hepatectomy (PH), and the effect of gastric 17β-estradiol on the pituitary function was investigated. In the PVL rats, arterial 17β-estradiol increased 9.5 times that of controls on day 3, and gradually decreased near to control levels in the portal vein by 4 weeks, which was still 5 times higher than those in the arteries of the control rats. In the PH rats, arterial 17β-estradiol increased 2 times that of controls on day 3, and gradually decreased to the control levels. Regeneration and growth of the liver remnants were observed about 2 weeks after PH. In the PVL and PH animals, pituitary ERα and prolactin mRNAs levels increased, positively correlating with an increase of arterial 17β-estradiol levels. Both reduced LHβ mRNA. It is apparent that hepatic dysfunction causes changes in gastric 17β-estradiol levels in the systemic circulation; and that elevated gastric 17β-estradiol affects pituitary function(s). This data suggest that gastric 17β-estradiol has a pivotal role in the regulation of the gastro-hepato-pituitary axis.
    Endocrine 07/2012; · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Immunoperoxidase method combined with cytofluorimetry showed that in contrast to hepatocytes, enhanced expression of prolactin receptors on rat cholangiocytes induced by common bile duct ligation cannot be suppressed by the prolactin secretion inhibitor bromocriptine.
    Bulletin of Experimental Biology and Medicine 01/1998; 126(1):687-689. · 0.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Expression of prolactin receptors (PR) in the nuclei and plasma membrane of the bile duct cells is demonstrated in 1-45-day-old male and female rats with the use of indirect immunoperoxidase technique. The intensity of PR staining in the bile duct cells is not sex-dependent; it increases from the 1st day till the 45th day and disappears by the 65th day of postnatal ontogeny. The PR-specific staining of hepatocytes also increases during the first 45 days of postnatal life and becomes sex-dependent by the 65th day.
    Bulletin of Experimental Biology and Medicine 12/1996; 122(6):1228-1231. · 0.34 Impact Factor