Bone sialoprotein plays a functional role in bone formation and osteoclastogenesis
2008; Rockefeller University Press; Volume: 205; Issue: 5 Linguagem: Inglês
10.1084/jem.20071294
ISSN1540-9538
AutoresLuc Malaval, Ndéye Marième Wade‐Gueye, Maya Boudiffa, Jia Fei, Ralph Zirngibl, Frieda Chen, Norbert Laroche, Jean‐Paul Roux, Brigitte Burt‐Pichat, F. Duboeuf, Georges Boivin, Pierre Jurdic, Marie‐Hélène Lafage‐Proust, Joëlle Amédée, Laurence Vico, Janet Rossant, Jane E. Aubin,
Tópico(s)Oral and Maxillofacial Pathology
ResumoBone sialoprotein (BSP) and osteopontin (OPN) are both highly expressed in bone, but their functional specificities are unknown. OPN knockout (-/-) mice do not lose bone in a model of hindlimb disuse (tail suspension), showing the importance of OPN in bone remodeling. We report that BSP(-/-) mice are viable and breed normally, but their weight and size are lower than wild-type (WT) mice. Bone is undermineralized in fetuses and young adults, but not in older (> or =12 mo) BSP(-/-) mice. At 4 mo, BSP(-/-) mice display thinner cortical bones than WT, but greater trabecular bone volume with very low bone formation rate, which indicates reduced resorption, as confirmed by lower osteoclast surfaces. Although the frequency of total colonies and committed osteoblast colonies is the same, fewer mineralized colonies expressing decreased levels of osteoblast markers form in BSP(-/-) versus WT bone marrow stromal cultures. BSP(-/-) hematopoietic progenitors form fewer osteoclasts, but their resorptive activity on dentin is normal. Tail-suspended BSP(-/-) mice lose bone in hindlimbs, as expected. In conclusion, BSP deficiency impairs bone growth and mineralization, concomitant with dramatically reduced bone formation. It does not, however, prevent the bone loss resulting from loss of mechanical stimulation, a phenotype that is clearly different from OPN(-/-) mice.
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