This research aims to thoroughly examine the effects of SRF on spinal cord injury (SCI) and its ability to significantly impact the recovery and regeneration of neuronal axons.
The researchers created rat models of SCI and scratch injury to primary spinal cord neurons to observe the expression of relevant factors after neuronal injury.
We found that the SRF, Ras, Raf, and cofilin levels increased after injury and gradually returned to normal levels. Afterward, researchers gave rats with SCI an SRF inhibitor (CCG1423) and studied the effects with nuclear magnetic resonance and transmission electron microscopy. The SRF inhibitor rodents had worse spinal cord recovery and axon regrowth than the control group. And the apoptosis of primary neurons after scratch injury was significantly higher in the SRF inhibitor group. Additionally, the researchers utilized lentiviral transfection to modify the SRF expression in neurons. SRF overexpression increased neuron migration while silencing SRF decreased it. Finally, Western blotting and RT-PCR were conducted to examine the expression changes of related factors upon altering SRF expression. The results revealed SRF overexpression increased Ras, Raf, and cofilin expression. Silencing SRF decreased Ras, Raf, and Cofilin expression.
Based on our research, the SRF promotes axonal regeneration by activating the \"Ras-Raf-Cofilin\" signaling pathway.
目的:本研究旨在全面检查SRF对脊髓损伤(SCI)的影响及其对神经元轴突恢复和再生的影响。
方法:研究人员建立大鼠脊髓损伤和脊髓初级神经元划痕损伤模型,观察神经元损伤后相关因子的表达。
结果:我们发现SRF,拉斯,Raf,伤后cofilin水平升高并逐渐恢复至正常水平。之后,研究人员给予SCI大鼠一种SRF抑制剂(CCG1423),并用核磁共振和透射电子显微镜研究了其作用.SRF抑制剂啮齿动物的脊髓恢复和轴突再生比对照组差。SRF抑制剂组划痕损伤后原代神经元的凋亡明显增高。此外,研究人员利用慢病毒转染改变SRF在神经元中的表达.SRF过表达增加了神经元的迁移,而沉默SRF则减少了神经元的迁移。最后,采用Westernblotting和RT-PCR检测SRF表达改变后相关因子的表达变化。结果显示SRF过表达增加了Ras,Raf,和cofilin表达式。沉默SRF降低了Ras,Raf,和Cofilin表达式。
结论:根据我们的研究,SRF通过激活“Ras-Raf-Cofilin”信号通路促进轴突再生。