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演題詳細

Oral

グリア
Glia

開催日 2014/9/11
時間 15:00 - 16:00
会場 Room J(313+314)
Chairperson(s) 小泉 修一 / Schuichi Koizumi (山梨大学大学院医学工学総合研究部薬理学講座 / Department of Neuropharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Japan)
津田 誠 / Makoto Tsuda (九州大学大学院薬学研究院ライフイノベーション分野 / Department of Life Innovation, Graduate School of Pharmaceutical Sciences, Kyushu University, Japan)

PDGFR-αの不活性化はOPCの分化、および間葉系幹細胞の動員とOPCへの分化を誘導する
PDGFR-α inactivation induces maturation of OPCs and recruitment and transdifferentiation of MSCs into OPCs

  • O1-J-4-3
  • 笹原 正清 / Masakiyo Sasahara:1 ダン チュン タン / Chung Thanh Dang:1 石井 陽子 / Yoko Ishii:1 濱島 丈 / Takeru Hamashima:1 山本 誠士 / Seiji Yamamoto:1 大川  宜昭 / Noriaki Ohkawa:2,3 斎藤 喜人 / Yoshito Saitoh:2,3 井ノ口 馨 / Kaoru Inokuchi:2,3 森 寿 / Hisashi Mori:4 
  • 1:富山大院・医・病態病理学 / Dept Pathol, Univ of Toyama, Toyama, Japan 2:富山大院・医・生化学 / Dept Biochem, Univ of Toyama, Toyama, Japan 3:科学技術振興機構 / CREST, Japan 4:富山大院・医・分子神経科学 / Dept Mol Neurosci, Univ of Toyama, Toyama, Japan 

For the maintenance and repair of CNS myelin, oligodendrocyte progenitor cells (OPCs) continue to proliferate and maturate into myelin-forming oligodendrocytes (OLs) in adult CNS. PDGFR-α is expressed in OPCs and is essential for the development of these cells. The present study was aimed to understand the cell turnover of adult OPCs and the role of PDGFR-α involved. PDGFR-α gene knockout (KO) was induced by giving tamoxifen (TM) to the adult mutant mouse harboring ubiquitous promoter-driven Cre recombinase. Few days after gene KO, the OPCs that show immature immuno-phenotype as positive PDGFR-α/NG2 staining mostly disappeared from entire part of CNS of the mutant. Subsequently, OPCs simultaneously repopulated at multiple sites of brain, and almost restored OPCs populations after 4 weeks. Within this sequence of events, we found that OPCs were transiently depleted because pre-existing OPCs subjected to gene KO quickly differentiated toward myelin-forming OLs. On the other hand, the repopulated OPCs were positive for mesenchymal stem cell (MSC) markers, and were suggested to originate from MSCs that escaped from TM-induced gene KO and were associated with blood vessels and meninges in lineage-tracing studies using GFP-expressing viral infection. Genetic mapping showed few MSCs were recruited from meninges and differentiated into OPCs in PDGFR-α preserving control CNS as well. It was shown that PDGFR-α was essential to maintain the adult OPCs, and that MSCs were potent cellular resources that can be recruited and can transdifferentiate into OPCs.

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