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.
Highlights
A variety of trauma can lead to peripheral nerve injury
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 Human mesenchymal stem cells (hMSCs)
Direct hMSCs transplantation has been examined as a therapeutic application
Summary
A variety of trauma can lead to peripheral nerve injury. According to the statistical report from U.S Department of Transportation, 2,313,000 people were injured from car accidents in 2013 [1]. A set of inflammatory activities were initiated to promote the newly recruited glial cells to form supporting networks for axon regeneration [3,4,5]. The key to surgical repair of the transected nerve is to bridge the lesion with either autologous nerve graft [6], or synthetic nerve graft [7] for the local axon to rejoin. Advanced technologies such as a drug loaded hydrogel [8], decellularized tissue scaffold [9], and cell transplantation [10] have been incorporated into conduit design for nerve repair. With the development of stem cell based technology, using stem cell to repair damaged neural tissues as an alternative of autologous Schwann cells has become more applicable [12]
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