Document Type
Article
Publication Date
6-28-2017
Department
Department of Biomedical Engineering
Abstract
Development of successful clinical treatments for peripheral nerve injury is limited due to the complications behind neural physiology. Human mesenchymal stem cells (hMSCs) have the ability to directly promote tissue repair and protect cells at the injury site. Studies have shown that hMSCs can be transplanted to improve nerve regeneration. Hypoxic culture condition has been proven to maintain the stemness of hMSCs for later differentiation. In this study, we investigated the effects of low oxygen (O2) (2% and 5% O2) pre-treatment and initial seeding density (500, 1000, and 2000 cells/cm2) on glial protein expression during glial differentiation of hMSCs. Results showed that the secretion of glial proteins was tunable by modifying the seeding density. Moreover, glial induction of hMSCs, characterized by the glial fibrillary acidic protein (GFAP) and S100β expressing phenotype, were enhanced by short-term hypoxia pretreatment. The significantly increased gene expression, including GFAP (10 folds in 2% O2, 25 folds in 5% O2), 2’,3’-Cyclic Nucleotide 3’ Phosphodiesterase (CNP) (600 folds in 2% O2, 800 folds in 5% O2), and neural growth factor receptor (NGFR) (4 folds in 5% O2), indicated that low oxygen, especially 5% O2 pretreated hMSCs had an improved potential for peripheral nerve regeneration.
Publication Title
AIMS Cell and Tissue Engineering
Recommended Citation
Qian, Z.,
Xing, Q.,
Fase, C.,
Jansen, K.,
&
Zhao, F.
(2017).
Effects of short term hypoxia-preconditioning on glial phenotype induction of human mesenchymal stem cells.
AIMS Cell and Tissue Engineering,
1(1), 47-63.
http://doi.org/10.3934/celltissue.2017.1.47
Retrieved from: https://digitalcommons.mtu.edu/michigantech-p/1317
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Version
Publisher's PDF
Publisher's Statement
© 2017 Feng Zhao, et al., licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0). Publisher’s version of record: https://doi.org/10.3934/celltissue.2017.1.47