PTBP-1 and TNF-α/NF-κB are involved in repair mechanisms of human umbilical cord mesenchymal stem cell transplantation in mice with spinal cord injury

PTBP-1和TNF-α/NF-κB参与人脐带间充质干细胞移植修复小鼠脊髓损伤机制

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作者:Hua Cao, Xiaofei Ji, Qi Wang, Xin Guan, Wenjuan Wei, Ying Li, Wei Zou, Jing Liu

Conclusions

hUC-MSC transplantation can protect neuron survival, promote myelin repair, and control glial scar formation in SCI mice.

Methods

Thoracic spinal cord hemisection injuries were performed on adult female Kunming mice. The mice with spinal cord injury (SCI) were injected with hUC-MSCs suspended in normal saline, while the control mice received an equal volume of normal saline. The histological HE staining and Nissl staining were performed 4 and 8 weeks after hUC-MSC transplantation in SCI mice. The Basso-Beattie-Bresnahan (BBB) locomotor rating scale was used to assess functional recovery after SCI. Western blotting was performed to determine the protein expressions.

Results

hUC-MSCs transplantation decreased cavitation and tissue loss and increased the number of Nissl bodies in the damaged areas of the spinal cord after 4 and 8 weeks. The BBB locomotor performance of the transplanted mice was significantly improved (P<0.01). The wet weight of the injured side of the gastrocnemius muscle was significantly higher in the transplant group than that in the control group. Western blotting showed that TUJ1 and Olig2 expressions were significantly higher in hUC-MSC-grafted mice than those in vehicle controls. Three days after hUC-MSC transplantation, the expressions of TNF-α and NF-κB were higher in MSC-grafted mice than those in vehicle controls. However, 4 weeks after stem cell transplantation, the expressions of these two factors decreased in hUC-MSC-grafted mice compared with those in the vehicle controls. At 8 weeks after hUC-MSC transplantation, the expression of PTBP-1 was decreased in hUC-MSC-grafted mice compared with that in vehicle controls. Conclusions: hUC-MSC transplantation can protect neuron survival, promote myelin repair, and control glial scar formation in SCI mice.

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