Deficiency in Androgen Receptor Aggravates Traumatic Brain Injury-Induced Pathophysiology and Motor Deficits in Mice

被引:5
|
作者
Chen, Yu-Hsin [1 ]
Chen, Yen-Chou [1 ]
Hwang, Ling-Ling [1 ]
Yang, Liang-Yo [2 ,3 ]
Lu, Dah-Yuu [4 ,5 ]
机构
[1] Taipei Med Univ, Coll Med, Grad Inst Med Sci, Taipei 11031, Taiwan
[2] China Med Univ, Coll Med, Sch Med, Dept Physiol, Taichung 40402, Taiwan
[3] China Med Univ Hosp, Dept Med Res, Lab Neural Repair, Taichung 40447, Taiwan
[4] China Med Univ, Sch Med, Dept Pharmacol, Taichung 404333, Taiwan
[5] Asia Univ, Dept Photon & Commun Engn, Taichung 404333, Taiwan
来源
MOLECULES | 2021年 / 26卷 / 20期
关键词
traumatic brain injury; controlled cortical impact; androgen receptor; ARKO mice; motor activity; ALPHA-II-SPECTRIN; CONTROLLED CORTICAL IMPACT; CEREBROSPINAL-FLUID; BREAKDOWN PRODUCTS; RAT MODEL; SIGNALING PATHWAY; PROTECTIVE ROLE; CELL-DEATH; BECLIN; AUTOPHAGY;
D O I
10.3390/molecules26206250
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Androgens have been shown to have a beneficial effect on brain injury and lower reactive astrocyte expression after TBI. Androgen receptors (ARs) are known to mediate the neuroprotective effects of androgens. However, whether ARs play a crucial role in TBI remains unknown. In this study, we investigated the role of ARs in TBI pathophysiology, using AR knockout (ARKO) mice. We used the controlled cortical impact model to produce primary and mechanical brain injuries and assessed motor function and brain-lesion volume. In addition, the AR knockout effects on necrosis and autophagy were evaluated after TBI. AR knockout significantly increased TBI-induced expression of the necrosis marker alpha-II-spectrin breakdown product 150 and astrogliosis marker glial fibrillary acidic protein. In addition, the TBI-induced astrogliosis increase in ARKO mice lasted for three weeks after a TBI. The autophagy marker Beclin-1 was also enhanced in ARKO mice compared with wild-type mice after TBI. Our results also indicated that ARKO mice showed a more unsatisfactory performance than wild-type mice in a motor function test following TBI. Further, they were observed to have more severe lesions than wild-type mice after injury. These findings strongly suggest that ARs play a role in TBI.
引用
收藏
页数:16
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