STC2 modulates ERK1/2 signaling to suppress adipogenic differentiation of human bone marrow mesenchymal stem cells
STC2 modulates ERK1/2 signaling to suppress adipogenic differentiation of human bone marrow mesenchymal stem cells
复制标题
STC2调节ERK1/2信号传导抑制人骨髓间充质干细胞的成脂分化
DOI：
10.1016/j.bbrc.2020.01.060
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发表时间：
2020-03-26
影响因子：
3.1
通讯作者：
Wang, Tao
中科院分区：
文献类型：
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作者：
Ma, Baicheng;Xu, Xiaoyuan;Wang, Tao
Stanniocalcin-2（STC2）是一种糖蛋白，发现在癌症，糖尿病和成骨的调节中起关键作用。在本文中，我们试图通过研究人类间充质干细胞（HMSC）脂肪生成分化的背景下STC2的重要性来扩展这些过去的研究，并探索了这种重要性的基础机制。我们发现，HMSC掺杂发生的第7天STC2表达显着降低。 When we deliberately overexpressed STC2 in these cells, this resulted in significantly decreased expression of both peroxisome proliferator-activated receptor gamma (PPAR gamma) and Fatty Acid Binding Protein-4 (FABP4) together with increased extracellular-signal regulated kinase 1/2 (ERK1/2) phosphorylation and markedly reduced lipid droplet formation within cells.使用ERK抑制剂U0126处理细胞的细胞破坏了这种ERK1/2磷酸化，并恢复了这些HMSC的脂肪分化。当我们击倒STC2表达时，观察到了相反的表型。因此，这些发现共同揭示了STC2在HMSC中调节ERK1/2信号传导，以抑制其脂肪分化。 （c）2020 Elsevier Inc.保留所有权利。
Stanniocalcin-2 (STC2) is a glycoprotein that has been found to play key roles in the regulation of cancer, diabetes mellitus, and osteogenesis. Herein we sought to extend these past studies by examining the importance of STC2 in the context of human mesenchymal stem cell (hMSC) adipogenic differentiation and exploring the mechanisms underlying such importance. We found that STC2 expression was significantly reduced on day 7 of hMSC adipogenesis. When we deliberately overexpressed STC2 in these cells, this resulted in significantly decreased expression of both peroxisome proliferator-activated receptor gamma (PPAR gamma) and Fatty Acid Binding Protein-4 (FABP4) together with increased extracellular-signal regulated kinase 1/2 (ERK1/2) phosphorylation and markedly reduced lipid droplet formation within cells. Treatment of cells using the ERK inhibitor U0126 disrupted this ERK1/2 phosphorylation and restored the adipogenic differentiation of these hMSCs. When we instead knocked down STC2 expression, the opposite phenotypes were observed. Together these findings thus reveal that STC2 modulates ERK1/2 signaling in hMSCs so as to suppress their adipogenic differentiation. (C) 2020 Elsevier Inc. All rights reserved.