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Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation

  • Authors:
    • Yibin Du
    • Shuo Zhang
    • Tao Yu
    • Gongwen Du
    • Hui Zhang
    • Zongsheng Yin
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedics, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China
    Copyright: © Du et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2473-2482
    |
    Published online on: August 1, 2016
       https://doi.org/10.3892/mmr.2016.5582
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Abstract

The present study aimed to determine whether co-culture with bone marrow‑derived endothelial progenitor cells (EPCs) affects the proliferation and differentiation of spinal cord-derived neural stem cells (NSCs), and to investigate the underlying mechanism. The proliferation and differentiation of the NSCs were evaluated by an MTT cell proliferation and cytotoxicity assay, and immunofluorescence, respectively. The number of neurospheres and the number of β‑tubulin III‑positive cells were detected by microscopy. The wingless‑type MMTV integration site family, member 3a (Wnt3a)/β-catenin signaling pathway was analyzed by western blot analysis and reverse transcription‑quantitative polymerase chain reaction to elucidate the possible mechanisms of EPC‑mediated NSC proliferation and differentiation. The results revealed that co‑culture with EPCs significantly induced NSC proliferation and differentiation. In addition, co‑culture with EPCs markedly induced the expression levels of Wnt3a and β‑catenin and inhibited the phosphorylation of glycogen synthase kinase 3β (GSK‑3β). By contrast, Wnt3a knockdown using a short hairpin RNA plasmid in the EPCs reduced EPC‑mediated NSC proliferation and differentiation, accompanied by inhibition of the EPC‑mediated expression of β‑catenin, and its phosphorylation and activation of GSK‑3β. Taken together, the findings of the present study demonstrated that Wnt3a was critical for EPC‑mediated NSC proliferation and differentiation.
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Copy and paste a formatted citation
Spandidos Publications style
Du Y, Zhang S, Yu T, Du G, Zhang H and Yin Z: Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation. Mol Med Rep 14: 2473-2482, 2016.
APA
Du, Y., Zhang, S., Yu, T., Du, G., Zhang, H., & Yin, Z. (2016). Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation. Molecular Medicine Reports, 14, 2473-2482. https://doi.org/10.3892/mmr.2016.5582
MLA
Du, Y., Zhang, S., Yu, T., Du, G., Zhang, H., Yin, Z."Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation". Molecular Medicine Reports 14.3 (2016): 2473-2482.
Chicago
Du, Y., Zhang, S., Yu, T., Du, G., Zhang, H., Yin, Z."Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation". Molecular Medicine Reports 14, no. 3 (2016): 2473-2482. https://doi.org/10.3892/mmr.2016.5582
Copy and paste a formatted citation
x
Spandidos Publications style
Du Y, Zhang S, Yu T, Du G, Zhang H and Yin Z: Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation. Mol Med Rep 14: 2473-2482, 2016.
APA
Du, Y., Zhang, S., Yu, T., Du, G., Zhang, H., & Yin, Z. (2016). Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation. Molecular Medicine Reports, 14, 2473-2482. https://doi.org/10.3892/mmr.2016.5582
MLA
Du, Y., Zhang, S., Yu, T., Du, G., Zhang, H., Yin, Z."Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation". Molecular Medicine Reports 14.3 (2016): 2473-2482.
Chicago
Du, Y., Zhang, S., Yu, T., Du, G., Zhang, H., Yin, Z."Wnt3a is critical for endothelial progenitor cell-mediated neural stem cell proliferation and differentiation". Molecular Medicine Reports 14, no. 3 (2016): 2473-2482. https://doi.org/10.3892/mmr.2016.5582
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