Exp Clin Endocrinol Diabetes 2006; 114(10): 584-589
DOI: 10.1055/s-2006-948310
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG · Stuttgart · New York

Expression and Distribution of Prolactin Receptor in Normal, Fibrotic, and Cirrhotic Human Liver

J. Simon-Holtorf 1 , H. Mönig 1 , H.-J. Klomp 2 , A. Reinecke-Lüthge 3 , U. R. Fölsch 1 , S. Kloehn 1
  • 1Department of Internal Medicine, University of Kiel, Germany
  • 2Department of Surgery, University of Kiel, Germany
  • 3Department of Pathology, University of Kiel, Germany
Further Information

Publication History

Received: May 17, 2006 First decision: June 21, 2006

Accepted: June 21, 2006

Publication Date:
19 December 2006 (online)

Abstract

Liver cirrhosis is often associated with elevated levels of prolactin (PRL). This is commonly attributed to impaired hepatic metabolism of estrogens. However, there is evidence suggesting that PRL may be an important factor in hepatic tissue regeneration. To investigate the role of PRL in the pathogenesis of liver cirrhosis, we used RT-PCR and immunhistochemical staining to analyze changes in the expression and the histological distribution of the prolactin receptor (PRLR) in normal, fibrotic and cirrhotic hepatic tissue. Liver tissue was obtained from 29 surgically explanted human livers. The histological examination demonstrated normal liver tissue (n=9) as well as different grades of fibrosis (n=10) and cirrhosis (n=10). In liver cirrhosis and fibrosis, PRLR-mRNA was expressed at a higher level compared to normal liver specimens. Immunohistochemical staining of normal liver tissue demonstrated homogeneous distribution of the PRLR in the hepatocytes and in the epithelial cells of the bile ducts. This pattern of distribution was lost in fibrosis, where an accumulation of the PRLR was observed in the damaged hepatocytes. As no PRL-mRNA was detectable in normal, fibrotic or cirrhotic tissue, PRL does not act through autocrine or paracrine mechanisms. These data confirm previous results, which we obtained using an animal model for experimental liver cirrhosis in rats suggesting a metabolic function of PRL in normal liver and a regenerative function in fibrotic and cirrhotic liver. In conclusion, PRL might be involved in the pathogenesis of liver cirrhosis.

References

Correspondence

Jan Simon-Holtorf, MD 

Department of Internal Medicine·University of Kiel

Schittenhelmstr. 12

24105 Kiel

Germany

Phone: +49/0/431/597 13 93

Fax: +49/0/431/597 13 02

Email: jsimonholtorf@1med.uni-kiel.de