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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.
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