Spinal cord injury (SCI) is one of serious traumatic diseases of the central nervous system and has no effective treatment because of its complicated pathophysiology. Tissue engineering strategy which contains scaffolds, cells, and growth factors can provide a promising treatment for SCI. Hydrogel that has 3D network structure and biomimetic microenvironment can support cellular growth and embed biological macromolecules for sustaining release. Dental pulp stem cells (DPSCs), derived from cranial neural crest, possess mesenchymal stem cell (MSC) characteristics and have an ability to provide neuroprotective and neurotrophic properties for SCI treatment. Basic fibroblast growth factor (bFGF) is able to promote cell survival and proliferation and also has beneficial effect on neural regeneration and functional recovery after SCI. Herein, a thermosensitive heparin-poloxamer (HP) hydrogel containing DPSCs and bFGF was prepared, and the effects of HP-bFGF-DPSCs on neuron restoration after SCI were evaluated by functional recovery tests, western blotting, magnetic resonance imaging (MRI), histology evaluation, and immunohistochemistry. The results suggested that transplanted HP hydrogel containing DPSCs and bFGF had a significant impact on spinal cord repair and regeneration and may provide a promising strategy for neuron repair, functional recovery, and tissue regeneration after SCI.

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Increasing evidence has confirmed that nigral iron accumulation and activation of NMDA receptors (NRs) contribute to the neurodegeneration of dopamine (DA) neurons in Parkinson's disease (PD). Earlier work indicated that activation of NRs participated in iron metabolism in the hippocampus. However, the relationship between activation of NRs and iron accumulation in DA neurons of the substantia nigra in PD was unknown. In this study, our results showed that NRs inhibitors MK-801 and AP5 protected nigrostriatal projection system and reduced nigral iron levels of 6-hydroxydopamine (6-OHDA)-induced PD rats. In vitro studies demonstrated that NMDA treatment increased the expression of iron importer divalent metal transporter 1 (DMT1) and decreased the expression of iron exporter ferropotin 1 (Fpn1), which were dependent on iron regulatory protein 1 (IRP1). This led to increased intracellular iron levels and intensified the decrease in mitochondrial transmembrane potential in MES23.5 dopaminergic neurons. In addition, we reported that MK801 and neuronal nitric oxide synthase inhibitor could antagonize 6-OHDA-induced up-regulation of IRP1 and DMT1 and down-regulation of Fpn1, thus attenuating 6-OHDA-induced iron accumulation in MES23.5 cells. This suggested that 6-OHDA-induced activation of NRs might modulate the expression of DMT1 and Fpn1 via the neuronal nitric oxide synthase-IRP1 pathway.-Xu, H., Liu, X., Xia, J., Yu, T., Qu, Y., Jiang, H., Xie, J., Activation of NMDA receptors mediated iron accumulation via modulating iron transporters in Parkinson's disease.