S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model.

Corneal disease was the most critical cause of vision loss. This study aimed to research a new method and provide a theoretical basis for treating corneal injury. A mice corneal epithelial injury model was constructed by the method of mechanical curettage. Models were treated with sphingosine 1-phosphate (S1P) and si-Spns2. An immunofluorescence assay was used to detect βIII-tubulin. The expressions of neurotrophic factor, S1P transporter, and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway-related proteins were detected by western blot. Hematoxylin-eosin staining was processed to detect the effect of SIP on corneal repair in mice. si-Spns2 inhibited the effect of S1P. S1P significantly repaired the corneal injury, while si-Spns2 treatment made it more severe. Moreover, S1P could significantly increase the levels of NGF, BDNF, GDNF, Spns2, and p-ERK1/2. si-Spns2 inhibits the effect of S1P in the expression of these proteins. S1P significantly increased axonal differentiation of trigeminal ganglion neurons, which was inhibited after si-Spns2 treatment. S1P promoted corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model. Treatment of corneal injury by S1P may be an effective approach.