| Autor: |
Zhou XY; Department of Neurology, First Affiliated Hospital of SoocChow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, China.; Department of Neurology, Lianyungang Hospital affiliated with Xuzhou Medical College, Tongguan Road 182, Lianyungang, Jiangsu, China., Hu DX; Department of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan, 430030, Hubei, China., Chen RQ; Department of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan, 430030, Hubei, China., Chen XQ; Department of Pathophysiology, School of Basic Medicine, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan, 430030, Hubei, China., Dong WL; Department of Neurology, First Affiliated Hospital of SoocChow University, 188 Shizi Street, Suzhou, 215006, Jiangsu, China. dwlsz8@163.com., Yi CL; Department of Traumatic Surgery, Tong-ji Hospital, Tong-ji Medical College, Huazhong University of Science and Technology, Jie Fang Avenue 1095, Wuhan, 430030, Hubei, China. chenglayi@163.com. |
| Abstrakt: |
Mammalian 14-3-3 isoforms exist predominantly in the brain and are heavily involved in neurological diseases. However, the isoform-specific role of 14-3-3 proteins in the brain remains largely unclear. Here, we investigated the role of 14-3-3 isoforms in rat brains after transient middle cerebral artery occlusion and reperfusion. 14-3-3β, η, γ and ζ but not ε or τ were selectively upregulated in cerebral cortical neurons after ischemia-reperfusion (I/R). Selectively, 14-3-3β, γ and ζ were translocated from cytoplasm into the nuclei of neurons after I/R. 14-3-3 bound to p65 and suppressed p65 expression in N2a cells. In the brain, 14-3-3 could either colocalize with p65 in the nuclei of neurons or segregate from p65 expression in cortical neurons after I/R. All evidence together suggests that 14-3-3 isoforms are differentially induced to enter into the nuclei of neurons after I/R, which might regulate NFκB signaling directly or indirectly. Since 14-3-3 proteins are essential for cell survival and NFκB is a key transcriptional factor, our data suggest that the 14-3-3/p65 signaling pathway might be a potential therapeutic target for stroke. |
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