Expression of type I, type II, and type X collagen genes during altered endochondral ossification in the femoral epiphysis of osteosclerotic (oc/oc) mice
Expression of type I, type II, and type X collagen genes during altered endochondral ossification in the femoral epiphysis of osteosclerotic (oc/oc) mice
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DOI：
10.1007/bf02685003
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发表时间：
2001-01-01
影响因子：
4.2
通讯作者：
Nagai, N
中科院分区：
文献类型：
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作者：
Yamasaki, A;Itabashi, M;Nagai, N
骨硬化（oc/oc）小鼠是一种基因上独特的小鼠突变，其破骨细胞具有功能缺陷，也患有佝偻病，并在骨骺生长板中显示出改变的软骨内成骨。该疾病的形态学特征是在出生后10天出现肥大软骨的异常延伸，随后（出生后21天）在血管侵入软骨细胞腔隙后并入干骺端编织骨而不破坏软骨基质。原位杂交显示，延长型肥大软骨细胞表达I型和II型胶原mRNA，以及X型胶原mRNA，干骺端成骨细胞除表达I型胶原mRNA外，还表达II型和X型胶原mRNA。信号的地形分布提示每种胶原基因在单个细胞中可能共表达。免疫组织化学显示，在延伸软骨和干骺端骨小梁中均可见I型、Il型和X型胶原蛋白的重叠沉积。这种异常的基因表达和胶原合成表明oc/oc小鼠股骨骨骺/干骺交界处的病理性骨化发生方式与正常软骨内骨化不同。这种异常可能不是由于骨骺板发育障碍，而是由于软骨转化为骨的失败，因为骨骺板本来是正常的，显示有序的分层区，并有软骨特异性基因的适当表达。
The osteosclerotic (oc/oc) mouse, a genetically distinct murine mutation that has a functional defect in its osteoclasts, also has rickets and shows an altered endochondral ossification in the epiphyseal growth plate. The disorder is morphologically characterized by an abnormal extension of hypertrophic cartilage at 10 days after birth, which is later (21 days after birth) incorporated into the metaphyseal woven bone without breakdown of the cartilage matrix following vascular invasion of chondrocyte lacunae. In situ hybridization revealed that the extending hypertrophic chondrocytes expressed type I and type II collagen mRNA, as well as that of type X collagen and that the osteoblasts in the metaphysis expressed type II and type X collagen mRNA, in addition to type I collagen mRNA, The topographic distribution of the signals suggests a possible coexpression of each collagen gene in the individual cells. Immunohistochemically, an overlapping deposition of type I, type Il, and type X collagen was observed in both the extending cartilage and metaphyseal bony trabeculae. Such aberrant gene expression and synthesis of collagen indicate that pathologic ossification takes place in the epiphyseal/metaphyseal junction of oc/oc mouse femur in different way than in normal endochondral ossification. This abnormality is probably not due to a developmental disorder in the epiphyseal plate but to the failure in conversion of cartilage into bone, since the epiphyseal plate otherwise appeared normal, showing orderly stratified zones with a proper expression of cartilage-specific genes.