ABSTRACT

Critical-size defects (CSDs) are challenging oral clinical issues that need to be solved. Adipose-derived mesenchymal stem cells (ADSCs) and gene therapy offer a new target to solve these issues. Consequently, ADSCs attract more and more attention because of advantages such as easy obtainability and no ethical concerns. TNF receptor-associated factor 6 (TRAF6) is a significant binding protein both of tumour necrosis factor superfamily and of the toll/interleukin-1 receptor superfamily. Evidence is accumulating that TRAF6 inhibited osteoclast formation and promoted the proliferation of multiple myeloma cell lines and bone resorption. Here, we reported that overexpression of TRAF6 enhanced the proliferation, migration and osteogenesis of ADSCs through Raf-Erk-Merk-Hif1a pathway. Cell sheet of ADSCs combined with TRAF6 accelerated the healing of CSDs. In a word, TRAF6 enhanced osteogenesis, migration and proliferation through Raf-Erk-Merk-Hif1a pathway.

摘要

临界尺寸缺陷 (CSD) 是具有挑战性的需要解决的口腔临床问题。脂肪来源的间充质干细胞 (ADSC) 和基因疗法为解决这些问题提供了新的靶点。因此，ADSCs 因其易于获得和无伦理问题等优点而受到越来越多的关注。TNF 受体相关因子 6 (TRAF6) 是肿瘤坏死因子超家族和 toll/interleukin-1 受体超家族的重要结合蛋白。越来越多的证据表明 TRAF6 抑制破骨细胞形成并促进多发性骨髓瘤细胞系的增殖和骨吸收。在这里，我们报道了 TRAF6 的过表达通过 Raf-Erk-Merk-Hif1a 通路增强了 ADSCs 的增殖、迁移和成骨。ADSC 的细胞片与 TRAF6 结合加速了 CSD 的愈合。