Background:

Spinal cord injury (SCI) causes devastating neurological damage, including secondary injuries dominated by neuroinflammation. The role of apelin, an endogenous ligand that binds the G protein-coupled receptor angiotensin-like receptor 1, in SCI remains unclear. Thus, our aim was to investigate the effects of apelin in inflammatory responses and activation of endogenous neural stem cells (NSCs) after SCI.

Methods:

Apelin expression was detected in normal and injured rats, and roles of apelin in primary NSCs were examined. In addition, we used induced pluripotent stem cells (iPSCs) as a carrier to prolong the effective duration of apelin and evaluate its effects in a rat model of SCI.

Results:

: Co-immunofluorescence staining suggested that apelin was expressed in both astrocytes and neurons. Following SCI, apelin expression decreased from 1–14 d and was re-upregulated at 28 d. Apelin promoted NSC proliferation and differentiation into neurons and oligodendrocytes. In vivo, lentiviral-transfected iPSCs were used as a carrier to prolong the effective duration of apelin. Transplantation of transfected iPSCs in situ immediately after SCI reduced activation of microglia and A1 astrocytes, facilitated recovery of motor function, and promoted the proliferation and differentiation of endogenous NSCs in rats.

Conclusion:

Apelin alleviated neuroinflammation and promoted the proliferation and differentiation of endogenous NSCs after SCI, suggesting that it might be a promising target for treatment of SCI.