Abstract
The endogenous spinal cord ependymal cells (SCECs), which form the central canal (CC), are critically involved in proliferation, differentiation and migration after spinal cord injury (SCI) and represents a repair cell source in treating SCI. Previously, we reported that BAF45D is expressed in the SCECs and the spinal cord neurons in adult mice and knockdown of BAF45D fail to induce expression of PAX6, a neurogenic fate determinant, during early neural differentiation of human embryonic stem cells. However, the effects of SCI on expression of BAF45D have not been reported. The aim of this study is to explore the expression and potential role of BAF45D in rat SCI model. In this study, adult rats were randomly divided into intact, sham, and SCI groups. We first explored expression of BAF45D in the SCECs in intact adult rats. We then explored SCI-induced loss of motor neurons and lesion of neurites in the anterior horns induced by the SCI. We also investigated whether the SCI-induced lesions in SCECs are accompanied by the motor neuron lesions. Finally, we examined the effect of BAF45D knockdown on cell growth in neuro2a cells. Our data showed that BAF45D is expressed in SCECs, neurons, and oligodendrocytes but not astrocytes in the spinal cords of intact adult rats. After SCI, the structure of CC was disrupted and the BAF45D-positive SCEC-derivatives were decreased. During the early stages of SCI, when shape of CC was affected but there was no disruption in circular structure of the SCECs, it was evident that there was a significant reduction in the number of neurites and motor neurons in the anterior horns compared with those of intact rats. In comparison, a complete loss of SCECs accompanied by further loss of motor neurons but not neurites was observed at the later stage. BAF45D knockdown was also found to inhibit cell growth in neuro2a cells. These results highlight the decreased expression of BAF45D in SCI-injured SCECs and the potential role of BAF45D downregulation in development of neuronal lesion after SCI in adult rats.
Highlights
Traumatic spinal cord injury (SCI) results in the death of neurons and glial cells, resulting in neurological deficits (Ahuja et al, 2017)
The results indicated that BAF45D is expressed in almost all the spinal cord ependymal cell (SCEC) (Figure 1E, arrows) and the neurons (Figure 1F, arrowhead)
We report the first expression profile of BAF45D in SCECs and spinal cord neurons in intact adult rats
Summary
Traumatic SCI results in the death of neurons and glial cells, resulting in neurological deficits (Ahuja et al, 2017). One potential therapeutic strategy for repairing SCI involves a combination of neuroprotective and neuroregenerative treatments via the use of NSCs (Assinck et al, 2017). Whether the transplantation of NSCs truly represents a viable clinical option, and can lead to the development of new therapeutic strategies for SCI, remains unclear (Assinck et al, 2017) and would require a deeper understanding of how the local environment influences neural repair (O’Shea et al, 2017) and whether we can develop novel combination strategies (Bunge, 2008; Becker et al, 2018). Recent developments in stem cell research have fueled the development of regenerative therapy using NSC transplantation, making it possible to rebuild the destroyed neural circuits (Zhu et al, 2018)
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