This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zinger, M. Articles by Ben-Jonathan, N. Search for Related Content PubMed PubMed Citation Articles by Zinger, M. Articles by Ben-Jonathan, N. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB ESTRADIOL PROGESTERONE

Prolactin Expression and Secretion by Human Breast Glandular and Adipose Tissue Explants

Departments of Cell Biology (M.M., N.B.-J.) and Obstetrics and Gynecology (M.Z.), University of Cincinnati, College of Medicine, Cincinnati, Ohio 45267

Address all correspondence and requests for reprints to: Dr. Nira Ben-Jonathan, Department of Cell Biology, 3125 Eden Avenue, Cincinnati, Ohio 45267-0521. E-mail: Nira.Ben-Jonathan{at}uc.edu.

Prolactin (PRL) is a 23-kDa hormone produced by the pituitary and extrapituitary sites. The main target of PRL is the breast, where it affects cellular growth, differentiation, and milk production. Recent evidence suggests that locally produced PRL plays a role in breast tumorigenesis. Our objective was to examine PRL synthesis/release in different tissues of the human breast and determine the effect of ovarian steroids. Breast tissue, obtained from women undergoing mastectomy or breast reduction, was separated into glandular (nonmalignant) and adipose explants and incubated for 10 d. Conditioned media were analyzed for PRL by a bioassay. PRL release from glandular explants decreased by 60% from d 1–3, followed by a 4-fold increase on d 10. PRL release from adipose explants was unchanged from d 1–3 and increased more than 10-fold by d 10. PRL gene expression, determined by RT-PCR, was low on d 0 and markedly increased on d 10 in both types of explants. De novo synthesis of PRL was confirmed by metabolic labeling. Progesterone suppressed PRL release from glandular explants without affecting adipose explants. Estradiol did not alter PRL release from either tissue. In conclusion, the human breast produces and releases bioactive PRL, with a higher release rate by adipose than glandular tissue. The time-dependent rise in PRL release suggests removal from inhibitory control. Progesterone may be one of the factors that suppresses PRL production in the glandular compartment, whereas the factor(s) that regulate adipose PRL are unknown. These data suggest an autocrine/paracrine role for PRL in human glandular and adipose breast tissue.

This investigation was funded by NIH Grants ES10154, CA80920, and RR08084; National Science Foundation Grant IBN-9974848; and a grant from the Elsa U. Pardee Foundation. Preliminary results of this investigation were presented at the 84th Annual Meeting of The Endocrine Society, San Francisco, California, June 2002.

M.Z. and M.M. contributed equally to this investigation.

Abbreviations: CM, Conditioned media; FBS, fetal bovine serum; GAPDH, glyceraldehyde-3-phospate dehydrogenase; H&E, hematoxylin and eosin; hPRL, human PRL; MTT, 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide; NRS, normal rabbit serum; PRL, prolactin; PRL-R, PRL receptor; UTR, untranslated region.

This article has been cited by other articles:

				E. R. Hugo, D. C. Borcherding, K. S. Gersin, J. Loftus, and N. Ben-Jonathan Prolactin Release by Adipose Explants, Primary Adipocytes, and LS14 Adipocytes J. Clin. Endocrinol. Metab., October 1, 2008; 93(10): 4006 - 4012. [Abstract] [Full Text] [PDF]

				N. Ben-Jonathan, C. R. LaPensee, and E. W. LaPensee What Can We Learn from Rodents about Prolactin in Humans? Endocr. Rev., February 1, 2008; 29(1): 1 - 41. [Abstract] [Full Text] [PDF]

				M. Kutsukake, R. Ishihara, M. Yoshie, H. Kogo, and K. Tamura Involvement of insulin-like growth factor-binding protein-related protein 1 in decidualization of human endometrial stromal cells Mol. Hum. Reprod., October 1, 2007; 13(10): 737 - 743. [Abstract] [Full Text] [PDF]

				U. A. White, A. A. Coulter, T. K. Miles, and J. M. Stephens The STAT5A-Mediated Induction of Pyruvate Dehydrogenase Kinase 4 Expression by Prolactin or Growth Hormone in Adipocytes Diabetes, June 1, 2007; 56(6): 1623 - 1629. [Abstract] [Full Text] [PDF]

				O. Eyal, J.-B. Jomain, C. Kessler, V. Goffin, and S. Handwerger Autocrine Prolactin Inhibits Human Uterine Decidualization: A Novel Role for Prolactin Biol Reprod, May 1, 2007; 76(5): 777 - 783. [Abstract] [Full Text] [PDF]

				C. R. LaPensee, N. D. Horseman, P. Tso, T. D. Brandebourg, E. R. Hugo, and N. Ben-Jonathan The Prolactin-Deficient Mouse Has an Unaltered Metabolic Phenotype Endocrinology, October 1, 2006; 147(10): 4638 - 4645. [Abstract] [Full Text] [PDF]

				A. Diogenes, A. M. Patwardhan, N. A. Jeske, N. B. Ruparel, V. Goffin, A. N. Akopian, and K. M. Hargreaves Prolactin Modulates TRPV1 in Female Rat Trigeminal Sensory Neurons J. Neurosci., August 2, 2006; 26(31): 8126 - 8136. [Abstract] [Full Text] [PDF]

				E. R. Hugo, T. D. Brandebourg, C. E. S. Comstock, K. S. Gersin, J. J. Sussman, and N. Ben-Jonathan LS14: A Novel Human Adipocyte Cell Line that Produces Prolactin Endocrinology, January 1, 2006; 147(1): 306 - 313. [Abstract] [Full Text] [PDF]

				V. Goffin, S. Bernichtein, P. Touraine, and P. A. Kelly Development and Potential Clinical Uses of Human Prolactin Receptor Antagonists Endocr. Rev., May 1, 2005; 26(3): 400 - 422. [Abstract] [Full Text] [PDF]