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Article first published online: 20 SEP 2012
Copyright © 2012 AlphaMed Press
Volume 30, Issue 10, pages 2234–2247, October 2012
How to Cite
Kako, E., Kaneko, N., Aoyama, M., Hida, H., Takebayashi, H., Ikenaka, K., Asai, K., Togari, H., Sobue, K. and Sawamoto, K. (2012), Subventricular Zone-Derived Oligodendrogenesis in Injured Neonatal White Matter in Mice Enhanced by a Nonerythropoietic Erythropoietin Derivative. STEM CELLS, 30: 2234–2247. doi: 10.1002/stem.1202
Author contributions: E.K. and N.K.: conception and design, collection and assembly of data, data analysis and interpretation, and manuscript writing; M.A.: conception and design and collection and assembly of data; H.H., K.A., H. Togari: conception and design; H. Takebayashi: provision of study material; K.I.: provision of study material; K. Sobue: conception and design and administrative support; K. Sawamoto: conception and design, financial support, data analysis and interpretation, and manuscript writing.
Disclosure of potential conflicts of interest is found at the end of this article.
First published online in STEM CELLSEXPRESS August 13, 2012.
- Issue published online: 20 SEP 2012
- Article first published online: 20 SEP 2012
- Accepted manuscript online: 13 AUG 2012 08:51AM EST
- Manuscript Accepted: 17 JUL 2012
- Manuscript Received: 6 DEC 2011
- Next Generation World-Leading Researchers
- International Human Frontier Science Program Organization
- Takeda Science Foundation
- Realization of Regenerative Medicine
- Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Niigata 951-8510, Japan
Additional Supporting Information may be found in the online version of this article.
|sc-11-1157_sm_SupplFigure1.jpg||797K||Supplemental Figure 1: Cell proliferation in the anterior and posterior SVZ following neonatal HI injury. (A-C) Cell proliferation in the SVZ following HI. Coronal sections of the aSVZ and pSVZ at P10 (5 days after HI) were immunostained for Ki67 (A, White broken lines indicate the wall of the lateral ventricle). The percentages of Ki67+ cells that were Ki67+Olig2+ newly generated OPCs were 33.8±4.3% (aSVZ) and 39.6±3.4% (pSVZ). The density of Ki67+ proliferating cells in the SVZ of the HI–injured hemisphere was significantly greater than that in the intact mice at P10 and P12 (B), (n=3, *P <0.05, **P <0.01, unpaired t-test) and showed significant increases in both the aSVZ and pSVZ at P10 (C), (n=3, *P <0.05, unpaired t-test). (D) Density of newly generated OPCs in the aSVZ. There was no significant difference in the density of BrdU+Olig2+ cells between the intact and HI-injured aSVZ at any time-point (P10, P13, or P17). Scale bar: 100 μm.|
|sc-11-1157_sm_SupplFigure2.jpg||312K||Supplemental Figure 2: Decreased number of proliferating Olig2+ cells in the SVZ during normal neonatal development. The density of BrdU+ newly generated Olig2+ cells in the aSVZ (A) and pSVZ (B). BrdU was intraperitoneally injected into wild-type mice 2 h before sacrifice, at P3, P5, P7, P10, P13, and P17. The densities of BrdU+Olig2+ cells at P3 were significantly higher than those at later stages in both the aSVZ and pSVZ. (n=3, *P <0.05, one-way ANOVA with Bonferroni's multiple comparison test).|
|sc-11-1157_sm_SupplFigure3.jpg||338K||Supplemental Figure 3: Differentiation of CFP+ cells into neuronal progenitors and astrocytes in the CC of Olig2CreERTM; Rosa26ECFP mice after HI. Brain sections of P13, P17, and P24 Olig2CreERTM; Rosa26ECFP mice exposed to HI at P5 and tamoxifen injection at P9 were immunostained for the new neuron marker Dcx or astrocyte marker GFAP. The percentage of CFP+ cells co-labeled with Dcx (A) or GFAP (B) in the CC was less than 10% at any time point, with no significant difference between the HI-exposed and intact groups.|
|sc-11-1157_sm_SupplFigure4.jpg||85K||Supplemental Figure 4: Knockdown of erythropoietin receptor (EPOR) by siRNA transfection in OPC culture. Q-RT-PCR for EPOR mRNA in OPCs cultured with negative control siRNA or EPOR-specific siRNA. Expression levels were normalized to those of GAPDH. The EPOR mRNA expression was suppressed significantly in the EPOR-specific siRNA-added OPC culture compared to that with negative control siRNA (n=5, *P<0.05, one-way ANOVA with Bonferroni's multiple comparison test).|
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