Biomedical Research · 2013 · 26 citations · 23 references
MedicinePathobiologyPathologyApoptosisBone MetabolismCartilage RepairBone DevelopmentBone FormationBone TissueCartilage BiologyCartilage BreakdownOsteoclast BiologyCartilage Degradation MechanismsCartilage HistopathologyCartilage MineralizationCartilaginous PortionHistochemical MarkersHistochemical MicroscopyTartrate-resistant Acid Phosphatase ActivityVascular Invasion Assessment
We have histologically examined vascular invasion and calcification of the hypertrophic zone during endochondral ossification in matrix metalloproteinase (MMP)-9 deficient (MMP-9-/-) mice and in their littermates at 3 days, 3 weeks and 6 weeks after birth. Capillaries and osteoclasts at the chondro-osseous junction showed an intense MMP-9 immunopositivity, suggesting that they recognize chemical properties of cartilaginous matrices, and then release MMP-9 for cartilage degradation. CD31-positive capillaries and tartrate-resistant acid phosphatase-reactive osteoclasts could be found in the close proximity in the region of chondro-osseous junction in MMP-9-/- mice, while in wild-type mice, vascular invasion preceded osteoclastic migration into the epiphyseal cartilage. Although MMP-9-/- mice revealed larger hypertrophic zones, the index of calcified area was significantly smaller in MMP-9-/- mice. Interestingly, the lower layer of the MMP-9-/- hypertrophic zone showed intense MMP-13 staining, which could not be observed in wild-type mice. This indicates that MMP-13 may compensate for MMP-9 deficiency at that specific region, but not to a point at which the deficiency could be completely rescued. In conclusion, it seems that MMP-9 is the optimal enzyme for cartilage degradation during endochondral ossification by controlling vascular invasion and subsequent osteoclastic migration.
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Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis
Gabriele Bergers, Rolf A. Brekken, Gerald McMahon et al. · Nature Cell Biology · 2000 · 2.8K citations · Full text
Medicine, Cancer Biology, Oncology +14