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Vu, Thiennu H; Shipley, J.Michael; Bergers, Gabriele; Berger, Joel E; Helms, Jill A; Hanahan, Douglas; Shapiro, Steven D; Senior, Robert M; Werb, Zena (1998)
Publisher: Elsevier BV
Journal: Cell
Languages: English
Types: Article
Subjects: Biochemistry, Genetics and Molecular Biology(all), Article
Homozygous mice with a null mutation in the MMP-9/ gelatinase B gene exhibit an abnormal pattern of skeletal growth plate vascularization and ossification. Although hypertrophic chondrocytes develop normally, apoptosis, vascularization, and ossification are delayed, resulting in progressive lengthening of the growth plate to about eight times normal. After 3 weeks post-natal, aberrant apoptosis, vascularization, and ossification compensate to remodel the enlarged growth plate and ultimately produce an axial skeleton of normal appearance. Transplantation of wild-type bone marrow cells rescues vascularization and ossification in gelatinase B–null growth plates, indicating that these processes are mediated by gelatinase B–expressing cells of bone marrow origin, designated chondro clasts. Growth plates from gelatinase B–null mice in culture show a delayed release of an angiogenic activator, establishing a role for this proteinase in controlling angiogenesis.
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