Loss of monocarboxylate transporter 1 aggravates white matter injury after experimental subarachnoid hemorrhage in rats.
10.1007/s11684-021-0879-9
- Author:
Xin WU
1
;
Zongqi WANG
1
;
Haiying LI
1
;
Xueshun XIE
1
;
Jiang WU
1
;
Haitao SHEN
1
;
Xiang LI
1
;
Zhong WANG
2
;
Gang CHEN
3
Author Information
1. Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
2. Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. wangzhong19640309@163.com.
3. Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. nju_neurosurgery@163.com.
- Publication Type:Journal Article
- Keywords:
microRNAs;
monocarboxylate transporter 1;
motor training;
subarachnoid hemorrhage;
white matter injury
- MeSH:
Animals;
Male;
MicroRNAs/genetics*;
Monocarboxylic Acid Transporters/genetics*;
Rats;
Rats, Sprague-Dawley;
Subarachnoid Hemorrhage;
Symporters/genetics*;
White Matter/injuries*
- From:
Frontiers of Medicine
2021;15(6):887-902
- CountryChina
- Language:English
-
Abstract:
Monocarboxylic acid transporter 1 (MCT1) maintains axonal function by transferring lactic acid from oligodendrocytes to axons. Subarachnoid hemorrhage (SAH) induces white matter injury, but the involvement of MCT1 is unclear. In this study, the SAH model of adult male Sprague-Dawley rats was used to explore the role of MCT1 in white matter injury after SAH. At 48 h after SAH, oligodendrocyte MCT1 was significantly reduced, and the exogenous overexpression of MCT1 significantly improved white matter integrity and long-term cognitive function. Motor training after SAH significantly increased the number of ITPR2
