Exendin-4 通过下调 RhoA 的表达和激活来促进肌动蛋白细胞骨架重排，并通过 PI3K 途径保护细胞免受 Nogo-A-Δ20 介导的扩展抑制和生长锥塌陷。
Exendin-4 promotes actin cytoskeleton rearrangement and protects cells from Nogo-A-Δ20 mediated spreading inhibition and growth cone collapse by down-regulating RhoA expression and activation via the PI3K pathway.
机构信息
Affiliated Hospital of the Logistics University of the Chinese People's Armed Police Force and Jinzhou Medical University Cooperative Training Center, Tianjin, 300162, China; Jinzhou Medical University, Jinzhou, Liaoning Province, 121001, China; Tianjin Key Laboratory of Neurotrauma Repair, Institute of Traumatic Brain Injury and Neuroscience, Center for Neurology and Neurosurgery, Affiliated Hospital of The Logistics University of the Chinese People's Armed Police Force, Tianjin, 300162, China.
Tianjin Key Laboratory of Neurotrauma Repair, Institute of Traumatic Brain Injury and Neuroscience, Center for Neurology and Neurosurgery, Affiliated Hospital of The Logistics University of the Chinese People's Armed Police Force, Tianjin, 300162, China.
出版信息
Biomed Pharmacother. 2019 Jan;109:135-143. doi: 10.1016/j.biopha.2018.10.008. Epub 2018 Nov 2.
Exendin-4 is a protein of the GLP-1 family currently used to treat diabetes. Recently, a greater number of biological properties have been associated with the GLP-1 family. Our data shows that exendin-4 treatment significantly increases the cytoskeleton rearrangement, which leads to an increasingly differentiated phenotype and reduced cell migration. We also found that exendin-4 could prevent SH-SY5Y and PC12 cells from Nogo-A-Δ20 mediated spreading inhibition and neurite collapse. Western blot analysis indicated that exendin-4 treatment both reduced the expression and activation of RhoA via the PI3K signaling pathway. These data suggest that exendin-4 may protect nerve regeneration by preventing the inhibition of Nogo-A via down-regulating RhoA expression and activation.
Exendin-4 是 GLP-1 家族的一种蛋白质，目前用于治疗糖尿病。最近，人们发现 GLP-1 家族具有更多的生物学特性。我们的数据表明，Exendin-4 处理可显著增加细胞骨架重排，从而导致表型分化增加和细胞迁移减少。我们还发现 Exendin-4 可防止 SH-SY5Y 和 PC12 细胞受到 Nogo-A-Δ20 介导的扩展抑制和轴突崩溃。Western blot 分析表明，Exendin-4 通过 PI3K 信号通路降低 RhoA 的表达和激活。这些数据表明，Exendin-4 可能通过下调 RhoA 的表达和激活来防止 Nogo-A 的抑制，从而保护神经再生。
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