期刊
JOURNAL OF NEUROCHEMISTRY
卷 126, 期 3, 页码 400-414出版社
WILEY
DOI: 10.1111/jnc.12207
关键词
Akt; apoptosis; blood-brain barrier; inflammation; stroke; TRAF5
资金
- National Natural Science Foundation of China [81100230, 81070089]
- National Science and Technology Support Project [2011BAI15B02, 2012BAI39B05]
- National Basic Research Program of China [2011CB503902]
- Special Funds for Basic Research and Operating Expenses of the Central Universities [4101032]
- Grants-in-Aid for Scientific Research [25670167, 23659404, 24390100] Funding Source: KAKEN
Tumor necrosis factor receptor-associated factor 5 (TRAF5) is an adaptor protein of the tumor necrosis factor (TNF) receptor superfamily and the interleukin-1 receptor/Toll-like receptor superfamily and plays important roles in regulating multiple signaling pathways. This study was conducted to investigate the role of TRAF5 in the context of brain ischemia/reperfusion (I/R) injury. Transient occlusion of the middle cerebral artery was performed on TRAF5 knockout mice (KO), neuron-specific TRAF5 transgene (TG), and the appropriate controls. Compared with the WT mice, the TRAF5 KO mice showed lower infarct volumes and better outcomes in the neurological tests. A low neuronal apoptosis level, an attenuated blood-brain barrier (BBB) disruption and an inhibited inflammatory response were exhibited in TRAF5 KO mice. TRAF5 TG mice exhibited an opposite phenotype. Moreover, the Akt/FoxO1 signaling pathway was enhanced in the ischemic brains of the TRAF5 KO mice. These results provide the first demonstration that TRAF5 is a critical mediator of I/R injury in an experimental stroke model. The Akt /FoxO1 signaling pathway probably plays an important role in the biological function of TRAF5 in this model.
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