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Demyelinating Disorders

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Blood-borne molecules promote oligodendrocyte precursor cell (OPC) proliferation in vitro

  • P1-327
  • 黒田 真里子 / Mariko Kuroda:1 村松 里衣子 / Rieko Muramatsu:1 山下 俊英 / Toshihide Yamashita:1 
  • 1:大阪大学大学院 / Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University 

Injury and inflammation in the brain and spinal cord cause demyelination, which contributes to neurological deficits. Remyelination is initiated by proliferation of oligodendrocyte precursor cells (OPCs) and supports recovery of neuronal function. In the present study, we explored the mechanism of OPC proliferation and found that blood-borne molecules enhance OPC proliferation in vitro. The OPCs were cultured in Dulbecco's Modified Eagle Medium containing transferrin, sodium pyruvate, bovine serum albumin, insulin, sodium selenite, biotin, hydrocortisone, platelet-drived growth factor, and fibroblast growth factor-2 from mouse brain at postnatal day 1. And the OPCs were treated with serum obtained from adult mice. We evaluated the ratio of 5'-Bromo-2-deoxyuridine (BrdU) incorporation into the OPCs. Treatment with mouse serum stimulated BrdU incorporation into the primary OPC, suggesting that serum contains cell proliferation factor. We investigated the molecular mechanism of cell proliferation by serum treatment and found that PI3 kinase /Akt and extracellular signal-regulated kinase (ERK) are required for serum-mediated OPC proliferation. These findings demonstrate that blood-borne molecules enhances OPC proliferation by a mechanism dependent on PI3K/Akt and ERK signaling, thus providing a new therapeutic strategy for the treatment of demyelinating disorders.

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