How vascular endothelial growth factor-A (VEGF) regulates differentiation of mesenchymal stem cells.
How vascular endothelial growth factor-A (VEGF) regulates differentiation of mesenchymal stem cells.
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DOI：
10.1369/0022155413516347
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发表时间：
2014-02
期刊：
影响因子：
--
通讯作者：
Olsen BR
中科院分区：
文献类型：
--
作者：
Berendsen AD;Olsen BR
血管内皮生长因子A（VEGF）是血管生成的关键因子，在骨骼发育和出生后体内平衡中起重要作用。VEGF作为软骨细胞的存活因子，并在软骨内骨化期间将软骨的吸收与骨形成偶联。最近，还发现它可以调节骨髓间充质干细胞成骨细胞和脂肪细胞分化之间的平衡。令人惊讶的是，VEGF的这种调节功能不是基于涉及细胞表面受体激活的旁分泌信号。相反，该机制似乎利用了细胞内VEGF，其在功能上与核膜蛋白核纤层蛋白A相关。核纤层蛋白A和VEGF分别通过调节成骨细胞和脂肪细胞转录因子Runx 2和PPARγ的水平来控制成骨细胞和脂肪细胞的分化。这些数据提出了一种有趣的可能性，即衰老过程中骨量的损失可能通过控制骨髓间充质干细胞中细胞内VEGF的水平和活性来操纵。
Vascular endothelial growth factor A (VEGF), a key factor in angiogenesis, plays an essential role in skeletal development and postnatal homeostasis. VEGF serves as a survival factor for chondrocytes and couples the resorption of cartilage with bone formation during endochondral ossification. Recently, it has also been found to regulate the balance between osteoblast and adipocyte differentiation in bone marrow mesenchymal stem cells. Surprisingly, this regulatory function of VEGF is not based on paracrine signaling involving cell surface receptor activation. Instead, the mechanism appears to utilize intracellular VEGF, which is functionally linked to the nuclear envelope protein lamin A. Lamin A and VEGF control osteoblast and adipocyte differentiation by regulating the levels of the osteoblast and adipocyte transcription factors Runx2 and PPARγ, respectively. These data raise the intriguing possibility that loss of bone mass during aging may be manipulated by controlling the levels and activity of intracellular VEGF in bone marrow mesenchymal stem cells.
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