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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Defective osteogenesis of the stromal stem cells predisposes CD18-null mice to osteoporosis
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Defective osteogenesis of the stromal stem cells predisposes CD18-null mice to osteoporosis

机译：基质干细胞的成骨性缺陷使CD18无小鼠易患骨质疏松症

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摘要

osteogenesis by the bone marrow stromal stem cells (BMSSCs) supports continuous bone formation and the homeostasis of the bone marrow microenvironment. The mechanism that controls the proliferation and differentiation of BMSSCs is not fully understood. Here, we report that CD18, a surface protein present primarily on hematopoietic cells, but not on differentiated mesenchymal cells, is expressed by the stromal stem cells and plays a critical role in the osteogenic process. Constitutive expression of CD18 on BMSSCs using a retroviral promoter significantly enhances bone formation in vivo, whereas genetic inactivation of CD18 in mice leads to defective osteogenesis due to decreased expression of the osteogenic master regulator Runx2/Cbfa1. The defective osteogenesis of the CD18-null BMSSCs can be restored by expressing full-length, but not cytoplasmic domain-truncated, CD18. Radiographic analyses with dual-energy x-ray absorptiometry and 3D microcomputed tomography show that mice lacking CD18 have decreased bone mineral density and exhibit certain features of osteoporosis. Altogether, this work demonstrates that CD18 functions critically in the osteogenesis of BMSSCs, and thus lack of CD18 expression in the leukocyte adhesion deficiency patients may predispose them to osteoporosis.
机译：骨髓基质干细胞（BMSSC）的成骨作用支持连续的骨形成和骨髓微环境的稳态。控制BMSSCs增殖和分化的机制尚未完全了解。在这里，我们报道CD18是一种表面蛋白，主要存在于造血细胞上，而不存在于分化的间充质细胞上，由基质干细胞表达，并在成骨过程中起关键作用。使用逆转录病毒启动子在BMSSCs上CD18的组成型表达显着增强了体内的骨形成，而小鼠中CD18的遗传失活由于成骨主调节因子Runx2 / Cbfa1的表达降低而导致成骨缺陷。可以通过表达全长但不被胞质域截短的CD18来恢复CD18缺失的BMSSC的成骨缺陷。使用双能X线吸收仪和3D微计算机断层扫描进行的放射线照相分析显示，缺少CD18的小鼠的骨矿物质密度降低，并表现出骨质疏松症的某些特征。总之，这项工作表明CD18在BMSSCs的成骨中起关键作用，因此白细胞粘附缺乏症患者CD18表达不足可能使他们容易患骨质疏松症。

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