Glial AP1 is activated with aging and accelerated by traumatic brain injury.
Glial AP1 is activated with aging and accelerated by traumatic brain injury.
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DOI：
10.1038/s43587-021-00072-0
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发表时间：
2021-07
期刊：
影响因子：
--
通讯作者：
Bonini NM
中科院分区：
文献类型：
--
作者：
Byrns CN;Saikumar J;Bonini NM
创伤性脑损伤后退行性疾病的出现通常被描述为正常年龄相关过程的加速。损伤后和老年人是否发生类似的分子过程尚不清楚。在这里，我们确定了一个功能动态和持久的神经胶质细胞转录反应，介导的保守的转录因子AP 1。在TBI后早期，胶质细胞AP 1对于恢复至关重要，确保大脑完整性和动物存活。与此形成鲜明对比的是，慢性AP1激活促进人类tau病理学、组织损失和死亡率。我们发现，随着年龄的增长，健康苍蝇的大脑也会激活类似的过程。在人类中，中度TBI后检测到AP1活性，并与小胶质细胞活化和tau病理学相关。我们的数据提供了对胶质细胞的关键分子见解，强调相同的分子过程驱动TBI中动态和矛盾的胶质细胞行为，可能还有年龄，首先起到保护作用，但长期促进疾病。
The emergence of degenerative disease after traumatic brain injury is often described as an acceleration of normal age-related processes. Whether similar molecular processes occur after injury and in age is unclear. Here we identify a functionally dynamic and lasting transcriptional response in glia, mediated by the conserved transcription factor AP1. In the early post-TBI period, glial AP1 is essential for recovery, ensuring brain integrity and animal survival. In sharp contrast, chronic AP1 activation promotes human tau pathology, tissue loss, and mortality. We show a similar process activates in healthy fly brains with age. In humans, AP1 activity is detected after moderate TBI and correlates with microglial activation and tau pathology. Our data provide key molecular insight into glia, highlighting that the same molecular process drives dynamic and contradictory glia behavior in TBI, and possibly age, first acting to protect but chronically promoting disease.
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影响因子：
11.2
作者：
Cole, James H.;Leech, Robert;Sharp, David J.
通讯作者：
Sharp, David J.
DOI：
10.1093/bioinformatics/btu638
发表时间：
2015-01-15
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
Anders S;Pyl PT;Huber W
通讯作者：
Huber W
影响因子：
64.5
作者：
Davie K;Janssens J;Koldere D;De Waegeneer M;Pech U;Kreft Ł;Aibar S;Makhzami S;Christiaens V;Bravo González-Blas C;Poovathingal S;Hulselmans G;Spanier KI;Moerman T;Vanspauwen B;Geurs S;Voet T;Lammertyn J;Thienpont B;Liu S;Konstantinides N;Fiers M;Verstreken P;Aerts S
通讯作者：
Aerts S
影响因子：
14.5
作者：
Arena, John D.;Smith, Douglas H.;Johnson, Victoria E.
通讯作者：
Johnson, Victoria E.
影响因子：
10.5
作者：
Chien, Yuchen;Scuoppo, Claudio;Lowe, Scott W.
通讯作者：
Lowe, Scott W.