دورية أكاديمية
Armcx1 Reduces Neurological Damage Via a Mitochondrial Transport Pathway Involving Miro1 After Traumatic Brain Injury.
العنوان: | Armcx1 Reduces Neurological Damage Via a Mitochondrial Transport Pathway Involving Miro1 After Traumatic Brain Injury. |
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المؤلفون: | Li Q; Department of Geriatrics, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China., Ni H; Department of Neurosurgery, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China; Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China., Rui Q; Department of Laboratory, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China., Ding J; Department of Neurosurgery, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China., Kong X; Department of Burn and Plastic Surgery, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China., Kan X; Department of Neurobiology and Anatomy, Xuzhou Key Laboratory of Neurobiology, Xuzhou Medical University, Xuzhou 221004, China., Gao R; Department of Neurosurgery, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China. Electronic address: gaorong_zjg@163.com., Shen H; Department of Geriatrics, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou 215600, China. Electronic address: shenhongboy@163.com. |
المصدر: | Neuroscience [Neuroscience] 2024 May 03; Vol. 545, pp. 111-124. Date of Electronic Publication: 2024 Mar 16. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Elsevier Science Country of Publication: United States NLM ID: 7605074 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7544 (Electronic) Linking ISSN: 03064522 NLM ISO Abbreviation: Neuroscience Subsets: MEDLINE |
أسماء مطبوعة: | Publication: [New York?] : Elsevier Science Original Publication: Oxford, Elmsford, N. Y., Pergamon Press |
مواضيع طبية MeSH: | Armadillo Domain Proteins*/metabolism , Brain Injuries, Traumatic*/metabolism , Brain Injuries, Traumatic*/pathology , Mice, Inbred C57BL* , Mitochondria*/metabolism , rho GTP-Binding Proteins*/metabolism, Animals ; Male ; Mice ; Adenosine Triphosphate/metabolism ; Apoptosis/physiology ; Disease Models, Animal ; Maze Learning/physiology ; Neurons/metabolism ; Neurons/pathology |
مستخلص: | Armcx1 is a member of the ARMadillo repeat-Containing protein on the X chromosome (ARMCX) family, which is recognized to have evolutionary conserved roles in regulating mitochondrial transport and dynamics. Previous research has shown that Armcx1 is expressed at higher levels in mice after axotomy and in adult retinal ganglion cells after crush injury, and this protein increases neuronal survival and axonal regeneration. However, its role in traumatic brain injury (TBI) is unclear. Therefore, the aim of this study was to assess the expression of Armcx1 after TBI and to explore possible related mechanisms by which Armcx1 is involved in TBI. We used C57BL/6 male mice to model TBI and evaluated the role of Armcx1 in TBI by transfecting mice with Armcx1 small interfering RNA (siRNA) to inhibit Armcx1 expression 24 h before TBI modeling. Western blotting, immunofluorescence, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, Nissl staining, transmission electron microscopy, adenosine triphosphate (ATP) level measurement, neuronal apoptosis analysis, neurological function scoring and the Morris water maze were performed. The results demonstrated that Armcx1 protein expression was elevated after TBI and that the Armcx1 protein was localized in neurons and astroglial cells in cortical tissue surrounding the injury site. In addition, inhibition of Armcx1 expression further led to impaired mitochondrial transport, abnormal morphology, reduced ATP levels, aggravation of neuronal apoptosis and neurological dysfunction, and decrease Miro1 expression. In conclusion, our findings indicate that Armcx1 may exert neuroprotective effects by ameliorating neurological injury after TBI through a mitochondrial transport pathway involving Miro1. (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.) |
فهرسة مساهمة: | Keywords: Armcx1; Miro1; apoptosis; mitochondria; traumatic brain injury |
المشرفين على المادة: | 8L70Q75FXE (Adenosine Triphosphate) 0 (Armadillo Domain Proteins) 0 (Miro-1 protein, mouse) EC 3.6.5.2 (rho GTP-Binding Proteins) 0 (Armcx1 protein, mouse) |
تواريخ الأحداث: | Date Created: 20240316 Date Completed: 20240427 Latest Revision: 20240507 |
رمز التحديث: | 20240508 |
DOI: | 10.1016/j.neuroscience.2024.03.009 |
PMID: | 38492796 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1873-7544 |
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DOI: | 10.1016/j.neuroscience.2024.03.009 |