Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function

[Objective:] To explore the role and mechanism of fibroblast growth factor 13 (FGF13) in the repair of inferior alveolar nerve injury. [Methods:] To establish the model of inferior alveolar nerve injury in SD (Sprague-Dawley) rats. RNA from inferior alveolar tissue samples was collected 1, 3, 7 days after injury. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to detect the transcription expression levels of FGF13 gene at different time points after injury. Primary trigeminal nerve cells of neonatal SD mice were extracted and divided into experimental group and control group, transfected with FGF13 overexpressed plasmid and control plasmid, respectively. 3 days after successful transfection, cell RNA was extracted to detect the gene expression level of neurotrophin by RT-qPCR. Trigeminal nerve cells were stained with Neun and βⅢ-Tubulin nerve immunofluorescence, and the axon length of nerve cells was observed by laser scanning confocal microscope. ND7/23 nerve cells were divided into overexpression group (ND7/23-FGF13) and control group (ND7/23-vector), transfected with FGF13 overexpression lentivirus and control virus, respectively. Stable transmutation strains were screened out by purinomycin, and FGF13 protein immunofluorescence staining and JC-1 mitochondrial membrane potential fluorescence probe staining were performed. Extract cell RNA, then RT-qPCR was used to detect the expression of mitophagy related genes. [Results:] The expression level of FGF13 was significantly increased at 1 day after inferior alveolar nerve injury, decreased at 3 days after injury, and decreased to an equivalent level to the control group at 7 days after injury. Compared with the control group, the expression of FGF13, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and other factors increased in the experimental group. In the lentivirus overexpression group, FGF13 protein was more densely distributed in the nucleus, mitochondrial membrane potential was significantly increased, and the expression of mitochondrial autophagy related genes was increased. [Conclusion:] After inferior alveolar nerve injury, the expression level of FGF13 is transiently increased, which may have potential significance for the repair process of inferior alveolar nerve. Overexpression of FGF13 in trigeminal nerve cells can promote axonal elongation of nerve cells. The underlying mechanism may be related to the regulation of mitochondrial function and the promotion of mitochondrial homeostasis.