Impaired bone fracture healing in matrix metalloproteinase-13 deficient mice
Impaired bone fracture healing in matrix metalloproteinase-13 deficient mice
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DOI：
10.1016/j.bbrc.2006.12.234
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发表时间：
2007-03-23
影响因子：
3.1
通讯作者：
D'Armiento, Jeanine
中科院分区：
文献类型：
--
作者：
Kosaki, Naoto;Takaishi, Hironari;D'Armiento, Jeanine
血管和细胞侵入软骨是骨折愈合的关键步骤。基质金属蛋白酶-13 (MMP-13) 是锌依赖性肽链内切酶家族的成员，在细胞外基质重塑中发挥重要作用。因此，我们研究了 MMP-13 在稳定骨折愈合的小鼠模型中的可能参与。 MMP-13 缺陷 (MMP-13(-/-)) 小鼠的骨折修复明显延迟，其特征是骨折愈伤组织中软骨吸收迟缓。免疫组织化学表明 MMP-13(-/-) 小鼠的骨折愈伤组织中存在血管穿透和破软骨细胞募集的严重缺陷。与观察结果一致，当 MMP13(-/-) 小鼠培养的软骨细胞沉淀与内皮细胞共培养时，其血管生成活性减弱。这些结果表明MMP-13对于骨折愈合过程中的血管生成过程至关重要，特别是在软骨吸收过程中。 (c) 2007 Elsevier Inc. 保留所有权利。
Vascular and cellular invasion into the cartilage is a critical step in the fracture healing. Matrix metalloprotemase-13 (MMP-13) is a member of the zinc-dependent endopeptidase family and plays an important role in remodeling of extracellular matrix. Therefore we investigated the possible involvement of MMP-13 in a murine model of stabilized bone fracture healing. Repair of the fracture in MMP-13 deficient (MMP-13(-/-)) mice was significantly delayed and characterized by a retarded cartilage resorption in the fracture callus. Immunohistochemistry indicated severe defects in vascular penetration and chondroclast recruitment to the fracture callus in MMP-13(-/-) mice. Consistent with the observations, the chondrocyte pellets cultured from the MMP13(-/-) mice exhibited diminished angiogenic activities when the pellets were co-cultured with endothelial cells. These results suggest that MMP-13 is crucial to the process of angiogenesis during healing of fracture, especially in the cartilage resorption process. (c) 2007 Elsevier Inc. All rights reserved.