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Background. Spinal cord injury (SCI) remains a challenge owing to limited therapies. The exosome of neural stem cells (NSCs-Exos) and FTY720 transplantation could improve SCI effectively. However, the effect and mechanism of NSCs-Exos combined with FTY720 (FTY720-NSCs-Exos) transplantation in the treatment of SCI are not fully understood. Methods. Sprague Dawley rats (8-week-old) were used to establish the SCI model, followed by the treatment of NSCs-Exos, FTY720, and FTY720-NSCs-Exos. The effect of FTY720, NSCs-Exos, and FTY720-NSCs-Exos combination treatment on hindlimb function, pathological changes, apoptosis activity, and the expression of spinal edema-related proteins and apoptosis-related proteins in SCI models were investigated by BBB scoring, HE staining, TUNEL staining and immunohistochemistry, and Western blotting. Meanwhile, the effect of these treatments on spinal cord microvascular endothelial cells (SCMECs) was detected under hypoxic circumstance. Results. Our results found that FTY720-NSCs-Exos could alleviate pathological alterations and ameliorate the hindlimb function and oxygen insufficiency in model mice after SCI. In addition, exosomes could ameliorate the morphology of neurons, reduce inflammatory infiltration and edema, decrease the expression of Bax and AQP-4, upregulate the expression of claudin-5 and Bcl-2, and inhibit cell apoptosis. At the same time, in vitro experiments showed that FTY720-NSCs-Exos could protect the barrier of SCMECs under hypoxic circumstance, and the mechanism is related to PTEN/AKT pathway. Conclusion. FTY720-NSCs-Exos therapy displayed a positive therapeutic effect on SCI by regulating PTEN/AKT pathway and offered a new therapy for SCI.

The tetraspanin CD63 has been described to have critical roles in multiple biological processes, including tumorigenesis and metastasis in several types of cancer. However, its role in esophageal carcinoma (EC) has not been reported. In the current study, immunohistochemistry was used to investigate CD63 expression in 106 esophageal cancer samples, 49 adjacent esophagus tissues and 17 normal esophagus mucosa tissues. The results revealed that the overexpression of CD63 was observed in esophageal cancer samples and negatively correlated with tumor stage and lymph node metastasis. To further evaluate the role of CD63 in esophageal carcinoma, the invasiveness of EC cells was analyzed using matrigel invasion assays and wound healing assays in vitro. Furthermore, it was found that CD63 knockdown increased the invasiveness of TE-1 cells through the upregulation of matrix metalloproteinase (MMP) expression via promoting epithelial-mesenchymal transition. The current data therefore suggested that low levels of CD63 expression may be involved in the tumor progression of esophageal carcinoma.