碩士 / 國立嘉義大學 / 生化科技學系研究所 / 102 / Abstract
Traumatic brain injury (TBI) is one of the most prevalent causes of mortality and morbidity in industrial society, yet its treatment might result in death and huge medical and social expenses. Adult neurogenesis mainly occurs in the subgranular zone of the hippocampal dentate gyrus, and can be modulated by certain physiological and pathological events. Sonic hedgehog (Shh) is a soluble secreted glycoprotein, binding to its receptor, Patched (Ptch), and leads to the activation of the transcription factor Gli1. Shh is important for the developing nervous systems, neuronal proliferation, differentiation, and survival. Mitogen-activated protein kinases (MAPKs) pathway is believed to responsible for the cell signaling triggering these processes. Our previous study has demonstrated that MAPK cascade is involved in TBI-induced neurogenesis. In this study, we want to evaluate the role of Shh on TBI-induced neurogenesis and its possible mechanisms. We found that the expression of Shh significantly increased at 8 hour after TBI. Administration of Shh antisense oligonucleotide not only significantly attenuated the Shh expression and MAPK cascade phosphorylation after TBI, but also decreased the level of hippocampal neurogenesis. In summary, these results suggest Shh plays an important role on the TBI-induced neurogenesis in hippocampus.
Keywords: traumatic brain injury, hippocampus, neurogenesis, sonic
hedgehog
| Identifer | oai:union.ndltd.org:TW/102NCYU5103001 |
| Creators | 廖姿毓 |
| Contributors | Yi-Ling Yang, 楊奕玲 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 0 |
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