2023 神醫中心學術演講4 (實體)
日期 : 5月 23日星期二
時間 : 上午11:00
地點 : 國衛院竹南院區/ 行政大樓B1第6會議室
主題 :Investigating nerve regeneration following traumatic brain injury
講師 :Jian-Ying Chuang (莊健盈) Ph.D.
教授兼副院長
臺北醫學大學神經醫學博士學位學程、國際神經醫學碩士學位學程
報名連結
摘要
Traumatic brain injury (TBI) may lead to long-term behavioural deficiency, especially secondary axotomy/axon degeneration induced caused by TBI is considered as a key risk factor of the early onset of neurodegenerative diseases. We recently discovered that zinc finger protein 179 (Znf179), also known as RING finger protein 112, acts as a novel neuroprotector and interacts with sigma-1 receptor (Sig-1R). After treatment with a Sig-1R agonist dehydroepiandrosterone sulfate, Znf179 increased its interaction with various cytoplasmic proteins, annotated to functions in “Protein Synthesis” and “Cellular Movement”. Interestingly, we found an obvious localization of Znf179 on neurite growth cones. Moreover, the Znf179-overexpressing transgenic mice had higher expression of genes involved in neural-regeneration compared to wild-type mice. Treatment with Sig-1R agonists used for Znf179 upregulation resulted in longer neurite outgrowth. In addition, we have known histone deacetylase 6 (HDAC6) as a binding partner of Znf179. Treatment with MPT0B291, a potent HDAC6 inhibitor, induced the association of Znf179 and the translation factors polyadenylate-binding protein-1 (PABP), which may stimulate translation initiation and promote protein synthesis. Therefore, in the study, we found that the HDAC6/Sig-1R/Znf179 pathway plays a pivotal role in axonal regeneration and functional recovery after traumatic axotomy. Using a pharmacological strategy-induced Znf179 functions via inhibiting HDAC6 activation and altering Sig-1R signaling can facilitate intrinsic regenerative outgrowth after TBI.
Key words: Znf179, Sig-1R, HDAC6, TBI, Neurite regeneration
會後合照
更新 : 2023-05-18
