MEC17 Induced α‐tubulin Acetylation Restores Mitochondrial Transport Function and Alleviates Axonal Injury after Intracerebral Hemorrhage in Mice

2021 ◽  
Author(s):  
Yang Yang ◽  
Xuezhu Chen ◽  
Zhizhong Feng ◽  
Xianfeng Cai ◽  
Xiaoming Zhu ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Axonal Injury ◽  
Transport Function ◽  
Mitochondrial Transport ◽  
Tubulin Acetylation

scholarly journals WldS and PGC-1  Regulate Mitochondrial Transport and Oxidation State after Axonal Injury

2013 ◽  
Vol 33 (37) ◽  
pp. 14778-14790 ◽  
Author(s):  
K. C. O'Donnell ◽  
M. E. Vargas ◽  
A. Sagasti
Keyword(s):  
Oxidation State ◽  
Axonal Injury ◽  
Mitochondrial Transport

Armcx1 Alleviates Secondary Brain Injury After Traumatic Brain Injury by Reducing Apoptosis and Axonal Injury in a Mouse Model of Controlled Cortical Impact

2021 ◽  
Author(s):  
Dengfeng Lu ◽  
Yi Wang ◽  
Guangjie Liu ◽  
Shixin Wang ◽  
Jing Wang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protein Level ◽  
Opposite Effect ◽  
Axonal Injury ◽  
Neurological Dysfunction ◽  
Secondary Brain Injury ◽  
Mitochondrial Transport ◽  
Controlled Cortical Impact ◽  
Cortical Impact

Abstract Armcx1 is highly expressed in the brain and is located in the mitochondrial outer membrane of neurons, where it mediates mitochondrial transport. Mitochondrial transport promotes the removal of damaged mitochondria and the replenishment of healthy mitochondria, which are essential for neuronal survival after traumatic brain injury (TBI). This study investigated the role of Armcx1 and its underlying regulator(s) in secondary brain injury (SBI) after TBI. An in vivo TBI model was established in C57BL/6 mice via controlled cortical impact (CCI). Adeno-associated viruses with Armcx1 overexpression and knockdown were constructed and administered to mice by stereotactic cortical injection. Exogenous miR-223-3P mimic or inhibitor was transfected into cultured cortical neurons, which were then scratched to simulate TBI in vitro. The Armcx1 protein level was found to be decreased in peri-lesion tissue, particularly in neurons. The overexpression of Armcx1 significantly reduced TBI-induced neurological dysfunction, apoptosis, axonal injury, and mitochondrial dysfunction, while knockdown of Armcx1 had the opposite effect. Armcx1 was a direct target of miR-223-3P. The miR-223-3P mimic significantly reduced the Armcx1 protein level, while the miR-223-3P inhibitor had the opposite effect. Finally, the miR-223-3P inhibitor significantly improved mitochondrial membrane potential and increased the total length of the neurites without affecting branching numbers, while the miR-223-3P mimic had the opposite effect. In summary, our results suggest that the decreased expression of Armcx1 protein in neurons after experimental TBI aggravates secondary brain injury, which may be regulated by miR-223-3P. Therefore, this study provides a potential therapeutic approach for treating TBI.

Traumatic or diffuse axonal injury? Author's response

2000 ◽  
Vol 26 (5) ◽  
pp. 491-491 ◽  
Author(s):  
J. F. Geddes ◽  
H. L. Whitwell ◽  
D. I. Graham
Keyword(s):  
Axonal Injury ◽  
Diffuse Axonal Injury

The Role of Stereotactic Technology in the Management of Intracerebral Hemorrhage

1992 ◽  
Vol 3 (3) ◽  
pp. 685-702 ◽  
Author(s):  
Christopher B. Shields ◽  
William A. Friedman
Keyword(s):  
Intracerebral Hemorrhage
Sign in / Sign up

Export Citation Format

Share Document