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TRAF6 participates in early brain injury after subarachnoid hemorrhage in rats through inhibiting autophagy and promoting oxidative stress
This study was designed to explore changes of expression level and potential roles and mechanisms of TRAF6 in early brain injury (EBI) after SAH by using a Sprague–Dawley rat model of SAH induced in 0.3 ml non‐heparinized autologous arterial blood injected into the prechiasmatic cistern. First, compared with the sham group, we found that the expression levels of TRAF6 increased gradually and peaked at 24 h after SAH. Second, the results showed that application of TRAF6 overexpression plasmid and genetic silencing siRNA could increase or decrease expression of TRAF6, respectively, and severely exacerbate or relieve EBI ...
Source: Journal of Neurochemistry - May 24, 2017 Category: Neurology Authors: Yang Dou, Haitao Shen, Dongxia Feng, Haiying Li, Xiaodi Tian, Jian Zhang, Zhong Wang, Gang Chen Tags: Original Article Source Type: research

Autophagy protects Human Brain Microvascular Endothelial Cells against Methylglyoxal‐induced Injuries: in parallel with Cerebral Ischemic Model in Diabetic Rats
This article is protected by copyright. All rights reserved.
Source: Journal of Neurochemistry - August 1, 2015 Category: Neurology Authors: Lili Fang, Xue Li, Yinbo Zhong, Jing Yu, Lina Yu, Haibin Dai, Min Yan Tags: Original Article Source Type: research

Ischemic neurons activate astrocytes to disrupt endothelial barrier via increasing VEGF expression
This article is protected by copyright. All rights reserved.
Source: Journal of Neurochemistry - November 20, 2013 Category: Neurology Authors: Ying‐Na Li, Rong Pan, Xu‐Jun Qin, Wei‐Lin Yang, Zhifeng Qi, Wenlan Liu, Ke Jian Liu Tags: Original Article Source Type: research

Calmodulin Kinase IV–dependent CREB activation is required for neuroprotection via NMDA receptor‐PSD95 disruption
This study highlights the importance of maintaining neuronal function following ischaemic injury. Future stroke research should target neurotrophic and pro‐survival signal pathways in the development of novel neuroprotective strategies. We propose that uncoupling NMDA receptors from PSD95 provides neuroprotection from stroke by enhancing Ca2+/Calmodulin‐dependent neurotrophic signalling. Blocking NMDAR‐PSD95 interactions allows enhanced activation of nuclear CaM‐kinase IV and prolonged phosphorylation of the CREB transcription factor, resulting in enhanced neurotrophic transcription. These findings demonstrate the...
Source: Journal of Neurochemistry - March 3, 2013 Category: Neurology Authors: Karen F. S. Bell, Russell J. Bent, Saira Meese‐Tamuri, Alicia Ali, Joan P. Forder, Michelle M. Aarts Tags: Original Article Source Type: research

Calmodulin Kinase IV‐dependent CREB activation is required for neuroprotection via NMDA receptor‐PSD95 disruption
This study highlights the importance of maintaining neuronal function following ischemic injury. Future stroke research should target neurotrophic and pro‐survival signal pathways in the development of novel neuroprotective strategies. © 2013 International Society for Neurochemistry, J. Neurochem. (2013) 10.1111/jnc.12176
Source: Journal of Neurochemistry - January 31, 2013 Category: Neurology Authors: Karen F. S. Bell, Russell J. Bent, Saira Meese‐Tamuri, Alicia Ali, Joan P. Forder, Michelle M. Aarts Tags: Original Article Source Type: research