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Publication : Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I.

First Author  Zhou Z Year  2000
Journal  Proc Natl Acad Sci U S A Volume  97
Issue  8 Pages  4052-7
PubMed ID  10737763 Mgi Jnum  J:61685
Mgi Id  MGI:1355423 Doi  10.1073/pnas.060037197
Citation  Zhou Z, et al. (2000) Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix metalloproteinase I. Proc Natl Acad Sci U S A 97(8):4052-7
abstractText  Membrane-type matrix metalloproteinase I (MT1-MMP)-deficient mice were found to have severe defects in skeletal development and angiogenesis. The craniofacial, axial, and appendicular skeletons were severely affected, leading to a short and domed skull, marked deceleration of postnatal growth, and death by 3 wk of age. Shortening of bones is a consequence of decreased chondrocyte proliferation in the proliferative zone of the growth plates. Defective vascular invasion of cartilage leads to enlargement of hypertrophic zones of growth plates and delayed formation of secondary ossification centers in long bones. In an in vivo corneal angiogenesis assay, null mice did not have angiogenic response to implanted FGF-2, suggesting that the defect in angiogenesis is not restricted to cartilage alone. In tissues from null mice, activation of latent matrix metalloproteinase 2 was deficient, suggesting that MT1-MMP is essential for its activation in vivo.
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