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Endocrinology Vol. 140, No. 1 96-105
Copyright © 1999 by The Endocrine Society

ARTICLES

Osteoblasts Are a New Target for Prolactin: Analysis of Bone Formation in Prolactin Receptor Knockout Mice1

Philippe Clément-Lacroix, Christopher Ormandy2, Liên Lepescheux, Patrick Ammann, Diane Damotte, Vincent Goffin, Brigitte Bouchard, Michael Amling, Martine Gaillard-Kelly, Nadine Binart, Roland Baron and Paul A. Kelly

INSERM U-344, Endocrinologie Moléculaire, Faculté de Médecine Necker (P.C.-L., V.G., B.B., N.B., P.A.K.), 75730 Paris Cedex 15, France; Cancer Research Program, Garvan Institute of Medical Research (C.O.), Darlinghurst, New South Wales 2010, Sydney, Australia; Hoechst Marion Roussel, Inc.-France (L.L., M.G.-K., R.B.), 93235 Romainville, France; the Division of Clinical Pathophysiology, World Health Organization Collaborating Center for Osteoporosis and Bone Diseases, Department of Internal Medicine, University Hospital (P.A.), Geneva, Switzerland; Service Anatomo-Pathologie, Hôpital Necker-Enfants Malades, Université René Descartes Paris V (D.D.), 75015 Paris, France; and the Departments of Cell Biology and Orthopedics, Yale University School of Medicine (M.A., R.B.), New Haven, Connecticut 06510

Address all correspondence and requests for reprints to: Dr. Paul A. Kelly, INSERM U-344, Endocrinologie Moléculaire, Faculté de Médecine Necker, 156 rue de Vaugirard, 75730 Paris Cedex 15, France. E-mail: kelly{at}necker.fr

Bone development is a multistep process that includes patterning of skeletal elements, commitment of hematopoietic and/or mesenchymental cells to chondrogenic and osteogenic lineages, and further differentiation into three specialized cell types: chondrocytes in cartilage and osteoblasts and osteoclasts in bone. Although PRL has a multitude of biological actions in addition to its role in the mammary gland, very little is known about its effect on bone. Mice carrying a germline null mutation for the PRL receptor gene have been produced in our laboratory and used to study the role of PRL in bone formation. In -/- embryos, we observed an alteration in bone development of calvaria. In adults, histomorphometric analysis showed that the absence of PRL receptors leads to a decrease in bone formation rate using double calcein labeling and a reduction of bone mineral density, measured by dual energy x-ray absorptiometry. In addition, serum estradiol, progesterone, testosterone, and PTH levels were analyzed. We also established that osteoblasts, but not osteoclasts, express PRL receptors. This suggests that an effect of PRL on osteoblasts could be required for normal bone formation and maintenance of bone mass. Thus, the PRL receptor knockout mouse model provides a new tool to investigate the involvement of PRL in bone metabolism.




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