Repair of spinal cord injury by chitosan scaffold with glioma ECM and SB216763 implantation in adult rats.

The loss of spinal cord tissue and the cavity formation are major obstacles to the repair of spinal cord injury (SCI). In the study, the scaffold of chitosan+ECM+SB216763 was fabricated and used for the repair of injured spinal cord injury. First, the biocompatibility of the scaffold was analyzed and results showed that the scaffold had a good compatibility with the neural stem cells. Especially, the processes of differentiated neural stem cell embedded in the scaffold were found in the experiment. At the same time, we also investigated the effect of scaffold on the differentiation of neural stem cell. The results showed that the scaffold of chitosan+ECM+SB216763 could significantly promote the differentiation of neural stem cells into neurons, astrocytes, and oligodendrocytes relative to those in other groups. In order to probe the application of scaffold in vivo, the rat models of spinal cord hemisection were set up and scaffolds were implanted into transected gap. Then the electrophysiology and BBB score were evaluated and results showed that the amplitude, latency period and BBB score in chitosan+ECM+SB216763 group were dramatically better than those in other groups. In addition, the differentiation of neural stem cells into nerve cells was also assayed and the results revealed that the number of neural stem cells differentiating into neuron, astrocytes and oligodendrocytes in chitosan+ECM+SB216763 group was significantly bigger than those in other groups. All these data suggested that the scaffold of chitosan+ECM+SB216763 would be a promising medium for the repair of injured spinal cord.

Serine protease inhibitor (SERPIN) B1 suppresses cell migration and invasion in glioma cells.

The serine protease inhibitor (SERPIN) B1 is expressed in numerous human tumors, but little is known regarding its role in the pathophysiology of glioma. In this paper, we report that SERPINB1 expression was down-regulated in high-grade human glioma tissue samples and glioblastoma cell lines. To investigate the role of SERPINB1 in glioma migration and invasion, we generated human glioma cell lines in which SERPINB1 was either overexpressed or depleted. Overexpression of SERPINB1 suppressed, while elimination of SERPINB1 promoted, the migration and invasion of glioma cells. SERPINB1 inhibited glioma migration and invasion probably by dampening the expression of matrix metalloproteinase-2 (MMP-2). Molecular data showed that the effect of SERPINB1 in glioma cells might be mediated via sustained inactivation of the phosphorylation of focal adhesion kinase (FAK) involved in the downregulation of the expressions of MMP-2. In a multivariate analysis, high SERPINB1 expression was showed to be associated with good prognosis in glioma. In conclusion, our data suggest that SERPINB1 negatively regulates glioma cell migration and invasion probably by abrogating the expression of MMP-2 and the activation of FAK. We suggest that SERPINB1 may offer the application in clinical medicine.