SHED repair critical-size calvarial defects in mice.
SHED repair critical-size calvarial defects in mice.
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DOI：
10.1111/j.1601-0825.2007.01396.x
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发表时间：
2008-07
期刊：
影响因子：
3.8
通讯作者：
Shi S
中科院分区：
文献类型：
--
作者：
Seo BM;Sonoyama W;Yamaza T;Coppe C;Kikuiri T;Akiyama K;Lee JS;Shi S
人类脱落型乳牙干细胞是一群高度增殖的出生后干细胞，能够分化为成牙本质细胞、脂肪细胞、神经细胞和骨诱导细胞。为了检验Share介导的骨再生是否可以用于治疗目的，我们使用Share修复了免疫受损小鼠的临界大小的颅骨缺损。建立颅骨缺损区，以羟基磷灰石/磷酸三钙为载体植入缺损区。Share能够修复大量的骨形成的缺损区。有趣的是，Share介导的成骨未能招募到骨髓间充质干细胞生成的骨中常见的造血型骨髓元素。此外，SHEAD还发现间充质干细胞标志物CC9/MUC18/CD146与一系列生长因子受体如转化生长因子β受体I和II、成纤维细胞生长因子受体I和III以及血管内皮生长因子受体I共表达，提示其具有综合分化潜能。我们的数据表明，来源于神经脊细胞的SHIP可能选择了独特的机制来发挥成骨作用。SHIP可能是一种较好的口腔面骨再生材料。
Stem cells from human exfoliated deciduous teeth (SHED) are a population of highly proliferative postnatal stem cells capable of differentiating into odontoblasts, adipocytes, neural cells, and osteo-inductive cells. To examine whether SHED-mediated bone regeneration can be utilized for therapeutic purposes, we used SHED to repair critical-size calvarial defects in immuno-compromised mice. We generated calvarial defects and transplanted SHED with hydroxyapatite/ tricalcium phosphate as a carrier into the defect areas. SHED were able to repair the defects with substantial bone formation. Interestingly, SHED-mediated osteogenesis failed to recruit hematopoietic marrow elements that are commonly seen in bone marrow mesenchymal stem cell-generated bone. Furthermore, SHED were found to co-express mesenchymal stem cell marker, CC9/MUC18/CD146, with an array of growth factor receptors such as transforming growth factor β receptor I and II, fibroblast growth factor receptor I and III, and vascular endothelial growth factor receptor I, implying their comprehensive differentiation potential. Our data indicate that SHED, derived from neural crest cells, may select unique mechanisms to exert osteogenesis. SHED might be a suitable resource for orofacial bone regeneration.
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