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Role of TAZ in Lysophosphatidic Acid-Induced Migration and Proliferation of Human Adipose-Derived Mesenchymal Stem Cells

机译:TAZ在溶血磷脂酸诱导的人脂肪间充质干细胞迁移和增殖中的作用

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摘要

Transcriptional co-activator with a PDZ-binding motif (TAZ) is an important factor in lysophosphatidic acid (LPA)-induced promotion of migration and proliferation of human mesenchymal stem cells (MSCs). The expression of TAZ significantly increased at 6 h after LPA treatment, and TAZ knockdown inhibited the LPA-induced migration and proliferation of MSCs. In addition, embryonic fibroblasts from TAZ knockout mice exhibited the reduction in LPA-induced migration and proliferation. The LPA1 receptor inhibitor Ki16425 blocked LPA responses in MSCs. Although TAZ knockdown or knockout did not reduce LPA-induced phosphorylation of ERK and AKT, the MEK inhibitor U0126 or the ROCK inhibitor Y27632 blocked LPA-induced TAZ expression along with the reduction in the proliferation and migration of MSCs. Our data suggest that TAZ is an important mediator of LPA signaling in MSCs in the downstream of MEK and ROCK signaling.
机译:具有PDZ结合基序(TAZ)的转录共激活因子是溶血磷脂酸(LPA)诱导的人类间充质干细胞(MSC)迁移和增殖促进的重要因素。 TPA的表达在LPA处理后6小时显着增加,而TAZ抑制可抑制LPA诱导的MSC迁移和增殖。此外,来自TAZ基因敲除小鼠的胚胎成纤维细胞显示LPA诱导的迁移和增殖减少。 LPA1受体抑制剂Ki16425阻断了MSC中的LPA反应。尽管TAZ敲除或敲除并没有减少LPA诱导的ERK和AKT磷酸化,但MEK抑制剂U0126或ROCK抑制剂Y27632阻止了LPA诱导的TAZ表达以及MSC增殖和迁移的减少。我们的数据表明,TAZ是MEK和ROCK信号下游的MSC中LPA信号的重要介体。

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