Smad3-dependent nuclear translocation of β-catenin is required for TGF-β1-induced proliferation of bone marrow-derived adult human mesenchymal stem cells
Smad3-dependent nuclear translocation of β-catenin is required for TGF-β1-induced proliferation of bone marrow-derived adult human mesenchymal stem cells
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DOI：
10.1101/gad.1388806
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发表时间：
2006-03-15
影响因子：
10.5
通讯作者：
Wang, XF
中科院分区：
文献类型：
--
作者：
Jian, HY;Shen, X;Wang, XF
来源于骨髓的成体间充质干细胞（MSC）有助于多种类型间充质组织的再生。在这里，我们描述了一种新的形式的串扰之间的转化生长因子β 1（TGF-β 1）和Wnt信号通路在调节人类骨髓间充质干细胞的活动的功能作用。我们发现TGF-β 1以Smad 3依赖的方式诱导MSC中β-连环蛋白的快速核转位。在功能上，该途径是刺激MSC增殖和TGF-β 1抑制MSC成骨细胞增殖所必需的，可能是通过调节特定的下游靶基因。这些结果为TGF-β和Wnt信号通路在这种特定的细胞环境中的新的合作模式提供了证据，并表明这种独特的信号通路在控制特定类型的MSC的自我更新和分化中具有潜在的重要作用。
Adult mesenchymal stem cells (MSCs) derived from bone marrow contribute to the regeneration of multiple types of mesenchymal tissues. Here we describe the functional role of a novel form of cross-talk between the transforming growth factor beta 1 (TGF-beta 1) and Wnt signaling pathways in regulating the activities of human MSCs. We show that TGF-beta 1 induces rapid nuclear translocation of beta-catenin in MSCs in a Smad3-dependent manner. Functionally, this pathway is required for the stimulation of MSC proliferation and the inhibition of MSC osteogenic differetiation by TGF-beta 1, likely through the regulation of specific downstream target genes. These results provide evidence for a new mode of cooperation between the TGF-beta and Wnt signaling pathways in this specific cellular context and suggest a potentially important role for this distinct signaling pathway in the control of self-renewal and differentiation of a specific type of MSCs.