The Journal of Experimental Medicine
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*Bone Marrow Transplantation
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© The Rockefeller University Press, 0022-1007/1999/2/729/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 4, February 15, 1999 729-734


Brief Definitive Reports

Cells Capable of Bone Production Engraft from Whole Bone Marrow Transplants in Nonablated Mice

Susan K. Nilsson*, Mark S. Dooner*, Heinz-Ulrich Weier{ddagger}, Baruch Frenkel*, Jane B. Lian*, Gary S. Stein*, and Peter J. Quesenberry*

From the * Cancer Center and the Department of Cell Biology, University of Massachusetts Medical Center, Worcester, Massachusetts 01605; and the {ddagger} Resource for Molecular Cytogenetics, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720

Allogeneic and autologous marrow transplants are routinely used to correct a wide variety of diseases. In addition, autologous marrow transplants potentially provide opportune means of delivering genes in transfected, engrafting stem cells. However, relatively little is known about the mechanisms of engraftment in transplant recipients, especially in the nonablated setting and with regard to cells not of hemopoietic origin. In particular, this includes stromal cells and progenitors of the osteoblastic lineage. We have demonstrated for the first time that a whole bone marrow transplant contains cells that engraft and become competent osteoblasts capable of producing bone matrix. This was done at the individual cell level in situ, with significant numbers of donor cells being detected by fluorescence in situ hybridization in whole femoral sections. Engrafted cells were functionally active as osteoblasts producing bone before being encapsulated within the bone lacunae and terminally differentiating into osteocytes. Transplanted cells were also detected as flattened bone lining cells on the periosteal bone surface.

Key Words: osteoprogenitors • osteoblasts • bone • bone marrow transplants • nonablated


Address correspondence to S.K. Nilsson at her present address, Sir Donald and Lady Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, Locked Bag No. 1, A'Beckett Street, Melbourne, 3000, Australia. Phone: 61-3-9656-1280; Fax: 61-3-9656-1411; E-mail: s.nilsson{at}pmci.unimelb.edu.au

P.J. Quesenberry was supported by grants from National Institutes of Diabetes and Digestive and Kidney Diseases (Nos. 49650-02 and 50222-01). H.-U. Weier was supported by a grant from the Office of Energy Research, Office of Environmental Research, US Department of Energy, under contract DE-AC-03-76SF00098. S.K. Nilsson is a CJ Martin Fellow, granted from the National Health and Medical Research Council (Australia), and is in part supported by the Our Danny Cancer Fund (University of Massachusetts, Worcester, MA).


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