Abstract
High-mobility group box 1 (HMGB1) facilitates neural stem cells (NSCs) proliferation and differentiation into neuronal linage. However, the effect of HMGB1 on NSCs migration is still elusive. The present study is to investigate the corelation between HMGB1 and NSCs migration and the potential mechanism. The results indicated that 1 ng/ml HMGB1 promoted NSCs proliferation using CCK8 assays. Moreover, data showed that 1 ng/ml HMGB1 facilitated NSCs migration via filopodia formation using phase-contrast and transwell assays. Furthermore, 1 ng/ml HMGB1 upregulated the expression of RAGE, one of the HMGB1 receptor, using western blotting assays and immunofluorescence staining. In addition, 1 ng/ml HMGB1 increased the percentage of filopodia formation using phalloidin staining. Meanwhile, the enhanced migration effect could be abrogated by 50 nM FPS-ZM1, one of the RAGE antagonist, and RAGE-specific siRNA through immunofluorescence and phalloidin staining. Together, our data demonstrate that HMGB1/RAGE axis facilitates NSCs migration via promoting filopodia formation, which might serve as a candidate for central nervous system (CNS) injury treatment and/or a preconditioning method for NSCs implantation.
Highlights
Neural stem cells (NSCs), one subtype of stem cells, hold promising regenerative therapeutic strategy as their capacity for self-renewal, migration toward lesions and differeniation into neurons, astrocytes and oligodendrocytes to restore the injuried regions following brain and spinal cord injury[1,2,3]
Considering that High-mobility group box 1 (HMGB1) holds the ability of inducing neural stem cells (NSCs) proliferation and differentiation, migration is another important factor for NSCs to restore lesions after injury
Results indicate that 1 ng/ml HMGB1 enhances NSCs proliferation, which is in line with previous study[17]
Summary
Neural stem cells (NSCs), one subtype of stem cells, hold promising regenerative therapeutic strategy as their capacity for self-renewal, migration toward lesions and differeniation into neurons, astrocytes and oligodendrocytes to restore the injuried regions following brain and spinal cord injury[1,2,3]. Into neurons in Alzheimer’s disease[17] and facilitates functional recovery, but not exacerbating inflammation via RAGE/Nuclear Factor-kappa B (NF-κB) axis after spinal cord injury[18]. Considering that HMGB1 holds the ability of inducing NSCs proliferation and differentiation, migration is another important factor for NSCs to restore lesions after injury. The present study finds an experimental answer to explain the potential mechanism through which NSCs spontaneously migration towards the lesions and might provide a suitable candidate following brain and spinal cord injury
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