| First Author | Wang L | Year | 2013 |
| Journal | J Neurochem | Volume | 126 |
| Issue | 3 | Pages | 400-14 |
| PubMed ID | 23413803 | Mgi Jnum | J:199630 |
| Mgi Id | MGI:5503300 | Doi | 10.1111/jnc.12207 |
| Citation | Wang L, et al. (2013) Tumor necrosis factor receptor-associated factor 5 is an essential mediator of ischemic brain infarction. J Neurochem 126(3):400-14 |
| abstractText | 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. |
