Histochemical aspects of the vascular invasion at the erosion zone of the epiphyseal cartilage in MMP-9-deficient mice
Histochemical aspects of the vascular invasion at the erosion zone of the epiphyseal cartilage in MMP-9-deficient mice
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DOI：
10.2220/biomedres.34.119
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发表时间：
2013-06-01
影响因子：
1.2
通讯作者：
Amizuka, Norio
中科院分区：
文献类型：
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作者：
Kojima, Taku;Hasegawa, Tomoka;Amizuka, Norio
我们对基质金属蛋白酶(MMP)-9缺陷（MMP-9(-/-)）小鼠及其窝仔在出生后3天、3周和6周的软骨内成骨过程中血管侵入和肥厚带钙化进行了组织学检查。软骨-骨交界处的毛细血管和破骨细胞显示出强烈的MMP-9免疫阳性，表明它们识别软骨基质的化学性质，然后释放MMP-9进行软骨降解。在MMP-9（-/-）小鼠中，cd31阳性的毛细血管和抗酒石酸磷酸酶反应性破骨细胞在软骨-骨连接处的位置非常接近，而在野生型小鼠中，血管入侵先于破骨细胞向骨骺软骨迁移。虽然MMP-9（-/-）小鼠的肥厚区较大，但MMP-9（-/-）小鼠的钙化区指数明显较小。有趣的是，MMP-9（-/-）肥厚带下层显示强烈的MMP-13染色，这在野生型小鼠中没有观察到。这表明MMP-13可以弥补该特定区域的MMP-9缺陷，但不能完全弥补缺陷的程度。综上所述，MMP-9似乎是软骨内成骨过程中软骨降解的最佳酶，通过控制血管侵入和随后的破骨细胞迁移。
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 MNP-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.