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首页> 外文期刊>Biochemical and Biophysical Research Communications >Pigment epithelium derived factor upregulates expression of vascular endothelial growth factor by human mesenchymal stem cells: Possible role in PEDF regulated matrix mineralization
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Pigment epithelium derived factor upregulates expression of vascular endothelial growth factor by human mesenchymal stem cells: Possible role in PEDF regulated matrix mineralization

机译：色素上皮衍生因子上调人间充质干细胞表达血管内皮生长因子：在PEDF调控基质矿化中的可能作用

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摘要

Pigment epithelium-derived factor (PEDF) encoded by serpinf1 is a potent antiangiogenic factor found in a wide variety of fetal and adult tissues. Several reports have shown that lack of PEDF leads to osteogenesis imperfecta (OI) type VI whose hallmark is a defect in mineralization that leads to excessive osteoid build up that fails to mineralize. Because PEDF is antiangiogenic factor it would pose serious consequences on bone development and healing of fractures. To understand possible mechanisms by which PEDF plays a role in bone development and regulation of matrix mineralization, we determined the effects of exogenous PEDF on vascular endothelial growth factor (VEGF) expression by human mesenchymal stem cells (hMSCs) and mechanisms of its regulation by PEDF. Human MSCs incubated in normal medium supplemented with exogenous PEDF increased VEGF expression; this increase was also seen when PEDF was added to hMSCs undergoing osteogenic differentiation. MSCs maintained in osteogenic medium increased synthesis of both VEGF and PEDF but both factors were maintained relatively in balance during differentiation. To understand mechanisms by which exogenous PEDF regulated VEGF expression, hMSCs exposed to PEDF activated Erk signaling pathway in MSCs; inhibition of Erk signaling reduced VEGF mRNA expression as well as protein production suggesting that PEDF regulates VEGF expression in MSCs via Erk signaling pathway. In conclusion, PEDF increases VEGF expression by MSCs suggesting that regulation of VEGF by PEDF may be part of the mechanisms by which PEDF regulates osteoblastic mineralization.
机译：serpinf1编码的色素上皮衍生因子（PEDF）是一种有效的抗血管生成因子，广泛存在于胎儿和成人组织中。几篇报道表明，缺乏PEDF会导致VI型成骨不全症（OI），其标志是矿化缺陷，导致过多的类骨质积聚而无法矿化。由于PEDF是抗血管生成因子，它将对骨骼发育和骨折愈合造成严重后果。为了了解PEDF在骨骼发育和基质矿化中发挥作用的可能机制，我们确定了外源PEDF对人间充质干细胞（hMSCs）血管内皮生长因子（VEGF）表达的影响以及PEDF对其调控的机制。在补充有外源PEDF的正常培养基中孵育的人MSC可增加VEGF的表达;当将PEDF加入经历成骨分化的hMSC中时，也可以看到这种增加。维持在成骨培养基中的MSC可以增加VEGF和PEDF的合成，但是在分化过程中，这两个因素均保持相对平衡。为了了解外源性PEDF调节VEGF表达的机制，暴露于PEDF的hMSC激活了MSC中的Erk信号通路。对Erk信号的抑制降低了VEGF mRNA的表达以及蛋白质的产生，这表明PEDF通过Erk信号通路调节MSC中的VEGF表达。总之，PEDF增加了MSC的VEGF表达，提示PEDF调节VEGF可能是PEDF调节成骨细胞矿化机制的一部分。

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