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...

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Main Authors: JIAO Yi, SUN Xinrong, LIU Weicai
Format: Article
Language:zho
Published: Editorial Office of Journal of Oral and Maxillofacial Surgery 2024-10-01
Series:Kouqiang hemian waike zazhi
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Online Access:https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2024.05.003
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author JIAO Yi
SUN Xinrong
LIU Weicai
author_facet JIAO Yi
SUN Xinrong
LIU Weicai
author_sort JIAO Yi
collection DOAJ
description [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.
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spelling doaj-art-7f2d8cc0e9bc4ca28855c3f55dab7d8d2025-08-25T06:11:20ZzhoEditorial Office of Journal of Oral and Maxillofacial SurgeryKouqiang hemian waike zazhi1005-49792024-10-0134534234910.12439/kqhm.1005-4979.2024.05.003Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial functionJIAO Yi0SUN Xinrong1LIU Weicai2Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Prosthodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai 200072, ChinaShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Prosthodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai 200072, ChinaShanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Prosthodontics, Stomatological Hospital and Dental School, Tongji University, Shanghai 200072, China[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.https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2024.05.003inferior alveolar nerve injuriesfibroblast growth factor 13mitochondria
spellingShingle JIAO Yi
SUN Xinrong
LIU Weicai
Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
Kouqiang hemian waike zazhi
inferior alveolar nerve injuries
fibroblast growth factor 13
mitochondria
title Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
title_full Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
title_fullStr Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
title_full_unstemmed Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
title_short Study on the role of FGF13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
title_sort study on the role of fgf13 in the repair of inferior alveolar nerve injury by regulating mitochondrial function
topic inferior alveolar nerve injuries
fibroblast growth factor 13
mitochondria
url https://journal06.magtech.org.cn/Jweb_joms/EN/10.12439/kqhm.1005-4979.2024.05.003
work_keys_str_mv AT jiaoyi studyontheroleoffgf13intherepairofinferioralveolarnerveinjurybyregulatingmitochondrialfunction
AT sunxinrong studyontheroleoffgf13intherepairofinferioralveolarnerveinjurybyregulatingmitochondrialfunction
AT liuweicai studyontheroleoffgf13intherepairofinferioralveolarnerveinjurybyregulatingmitochondrialfunction