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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix
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Impaired endochondral ossification and angiogenesis in mice deficient in membrane-type matrix

机译：缺乏膜型基质的小鼠软骨内骨化和血管生成受损

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摘要

Membrane-type matrix metalloproteinase l (MT1-MMP)-deficient mice were found to have severe defects in skeletal development and angiogenesis. The craniofacial, axial, and appendicular skele- tons 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 chondro- cyte 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.
机译：发现膜型基质金属蛋白酶l（MT1-MMP）缺陷小鼠在骨骼发育和血管生成中具有严重缺陷。颅面，轴向和阑尾骨骼受到严重影响，导致颅骨短而呈圆顶状，标志着出生后生长的减缓。和死亡3周龄。骨骼缩短是生长板增殖区软骨细胞增殖减少的结果。软骨的有害血管浸润导致生长板肥大区域的扩大和长骨中次生骨化中心的形成延迟。在体内角膜血管生成测定中。空小鼠对植入的FGF-2没有血管生成反应，这表明血管生成的缺陷不仅限于软骨。在无效小鼠的组织中，潜在基质金属蛋白酶2的激活不足，这表明MT1-MMP在体内对其激活至关重要。

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