この度、奈良先端科学技術大学院大学バイオサイエンス研究科の中島欽一教授に生体防御医学研究所でのセミナーをお願い致しました。
このセミナーでは、細胞外環境がエピゲノム制御を通して神経幹細胞の運命を決定する機構と、脊髄損傷モデルマウスにおけるHDAC阻害剤の治療効果について発表して頂きます。講演は英語で行われます。ご来聴を歓迎致します。
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演題 | Epigenetic regulation of neural stem cells by surrounding environment(seminar in English) |
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演者 | 中島 欽一 先生 奈良先端科学技術大学院大学バイオサイエンス研究科 教授
Prof. Kinichi NAKASHIMA Laboratory of Molecular Neuroscience,Graduate School of Biological Sciences, Nara Institute of Science and Technology |
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日時 | 平成23年6月17日(金)14時半より15時半まで
June 17 (Fri), 2011, 14:30-15:30
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場所 | 馬出医学系キャンパス内 生体防御医学研究所 本館1階 会議室
以下の地図の20番になります。 (http://www.kyushu-u.ac.jp/access/map/hospital/hospital.html)
Medical Institute of Bioregulation, Main Building 1F, Seminar Room
No.20 on the following linked map (http://www.kyushu-u.ac.jp/access/map/hospital/hospital-e.html)
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要旨 |
The mammalian embryonic brain contains multipotent neural stem cells (NSCs) that can self-renew and give rise to all three major cell types in the nervous system, i.e., neurons, astrocytes and oligodendrocytes. It has become apparent that epigenetic modifications of DNAs and histones play critical roles in fate specification of NSCs. In the first part of this talk, I will talk about DNA demethylation of astrocytic genes in NSCs is induced by Cell-Cell interaction with pregenerated neurons through the Notch signal activation in NSCs. This demethylation is also regulated by oxygen levels surrounding NSCs in the embryonic brain. In the second part, I will present data indicating that histone deacetylase inhibition induces neuronal differentiation of NSCs and its possible therapeutic application to the treatment of spinal cord injury.
- Namihira M et al. Committed neuronal precursors confer astrocytic potential on residual neural precursor cells. Dev Cell 16, 245-255, 2009
- Abematsu M et al. Neurons derived from transplanted neural stem cells restore disrupted neuronal circuitry in a mouse model of spinal cord injury.
J Clin Invest 120, 3255-3266, 2010
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連絡先 | 生体防御医学研究所 エピゲノム学 佐々木 裕之
Division of Epigenomics, MIB, Hiroyuki SASAKI 電話:092-642-6759 |
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