Zhan Peng, Xiong Hewei, Zheng Hongmei
Breast Cancer Center, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, National Key Clinical Specialty Discipline Construction Program, Hubei Provincial Clinical Research Center for Breast Cancer, Wuhan Clinical Research Center for Breast Cancer, Wuhan, Hubei, China, hust.edu.cn.
Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, tjmu.edu.cn.
Int J Genomics. 2025 Sep 23;2025:5520810. doi: 10.1155/ijog/5520810. eCollection 2025.
The purpose of this study was to investigate the role of the ITGB1/FAK/AKT pathway in NRG-1 in mediating the axonal growth of dorsal root ganglion neurons in Type I diabetic rats and to explore the mechanism of neuronal axonal regeneration. The effects of NRG-1 on neurite outgrowth in diabetic rats were determined by protein quantification and axon length analysis in which axons were identified with tubulin-III-specific staining. Western blot showed that the signaling activity of the ITGB1/FAK/AKT pathway was decreased in diabetic rats compared with normal rats, and exogenous NRG-1 significantly promoted axonal growth and activated the pathway. After the addition of ITGB1-specific siRNA, the axonal growth-promoting effect of NRG-1 was partially reversed. NRG-1 promotes axonal outgrowth in diabetic DRGs via upregulating the ITGB1/FAK/AKT pathway, providing a potential target for diabetic neuropathy.
本研究旨在探讨ITGB1/FAK/AKT通路在NRG-1介导I型糖尿病大鼠背根神经节神经元轴突生长中的作用,并探索神经元轴突再生的机制。通过蛋白质定量和轴突长度分析(其中轴突通过微管蛋白III特异性染色进行鉴定)来确定NRG-1对糖尿病大鼠神经突生长的影响。蛋白质印迹法显示,与正常大鼠相比,糖尿病大鼠中ITGB1/FAK/AKT通路的信号活性降低,外源性NRG-1显著促进轴突生长并激活该通路。添加ITGB1特异性小干扰RNA后,NRG-1的轴突生长促进作用部分逆转。NRG-1通过上调ITGB1/FAK/AKT通路促进糖尿病背根神经节的轴突生长,为糖尿病神经病变提供了一个潜在靶点。