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SPRY4 通过 MEK-ERK1/2 信号通路促进人骨髓间充质干细胞的成脂分化。

SPRY4 promotes adipogenic differentiation of human mesenchymal stem cells through the MEK-ERK1/2 signaling pathway.

机构信息

Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Center of Excellence in Tissue Engineering, Chinese Academy of Medical Sciences; Beijing Key Laboratory of New Drug Development and Clinical Trial of Stem Cell Therapy (BZ0381), P.R. China.

College of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang, P.R. China.

出版信息

Adipocyte. 2022 Dec;11(1):588-600. doi: 10.1080/21623945.2022.2123097.

DOI:10.1080/21623945.2022.2123097
PMID:36082406
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9481072/
Abstract

Obesity is a chronic metabolic disorder characterized by the accumulation of excess fat in the body. Preventing and controlling obesity by inhibiting the adipogenic differentiation of mesenchymal stem cells (MSCs) and thereby avoiding the increase of white adipose tissue is safe and effective. Recent studies have demonstrated that Sprouty proteins (SPRYs) are involved in cell differentiation and related diseases. However, the role and mechanism of SPRY4 in MSC adipogenic differentiation remain to be explored. Here, we found that SPRY4 positively correlates with the adipogenic differentiation of human adipose-derived MSCs (hAMSCs). Via gain- and loss-of-function experiments, we demonstrated that SPRY4 promotes hAMSC adipogenesis both in vitro and in vivo. Mechanistically, SPRY4 functioned by activating the MEK-ERK1/2 pathway. Our findings provide new insights into a critical role for SPRY4 as a regulator of adipogenic differentiation, which may illuminate the underlying mechanisms of obesity and suggest the potential of SPRY4 as a novel treatment option.

摘要

肥胖是一种慢性代谢性疾病，其特征是体内脂肪积累过多。通过抑制间充质干细胞（MSCs）的成脂分化来预防和控制肥胖，从而避免白色脂肪组织的增加，这是安全有效的。最近的研究表明，Sprouty 蛋白（SPRYs）参与细胞分化和相关疾病。然而，SPRY4 在 MSC 成脂分化中的作用和机制仍有待探索。在这里，我们发现 SPRY4 与人脂肪来源的间充质干细胞（hAMSCs）的成脂分化呈正相关。通过功能获得和功能丧失实验，我们证明 SPRY4 促进了 hAMSC 的体外和体内成脂分化。从机制上讲，SPRY4 通过激活 MEK-ERK1/2 通路发挥作用。我们的研究结果为 SPRY4 作为成脂分化调节剂的关键作用提供了新的见解，这可能阐明肥胖的潜在机制，并提示 SPRY4 作为一种新的治疗选择的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/2fee0a84d4df/KADI_A_2123097_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/575f90e85c40/KADI_A_2123097_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/81b66e8147ed/KADI_A_2123097_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/a6601d893e82/KADI_A_2123097_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/42fb0a40570d/KADI_A_2123097_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/3df478b6cc37/KADI_A_2123097_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/2fee0a84d4df/KADI_A_2123097_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/575f90e85c40/KADI_A_2123097_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/81b66e8147ed/KADI_A_2123097_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/a6601d893e82/KADI_A_2123097_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/42fb0a40570d/KADI_A_2123097_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/3df478b6cc37/KADI_A_2123097_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/9481072/2fee0a84d4df/KADI_A_2123097_F0006_OC.jpg

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Sprouty1 Prevents Cellular Senescence Maintaining Proliferation and Differentiation Capacity of Human Adipose Stem/Progenitor Cells.Sprouty1 可防止细胞衰老，维持人脂肪干细胞/祖细胞的增殖和分化能力。
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