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S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor
Chaoqun Lin1, Weina Li2, Xuezheng Fan1
1Department of Neurosurgery, University of Chinese Academy of Sciences-Shenzhen Hospital (Guangming District), Shenzhen 518106, Guangdong, China.
Abstract:
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.
Insights
Sphingosine 1-phosphate (S1P) significantly promotes corneal nerve repair and trigeminal neuron differentiation in mice. Blocking S1P transport with si-Spns2 worsens corneal injury, indicating S1P
Area of Science:
- Ophthalmology
- Neuroscience
- Regenerative Medicine
Background:
- Corneal disease is a leading cause of vision loss.
- Effective treatments for corneal injury and nerve regeneration are crucial.
Purpose of the Study:
- To investigate the therapeutic potential of sphingosine 1-phosphate (S1P) in corneal injury repair.
- To elucidate the role of S1P transporter (Spns2) in S1P-mediated corneal nerve regeneration.
Main Methods:
- Established a mouse corneal epithelial injury model.
- Treated models with S1P and si-Spns2 (inhibitor of Spns2).
- Assessed corneal repair using immunofluorescence (βIII-tubulin), Western blot (neurotrophic factors, Spns2, ERK1/2), and Hematoxylin-eosin staining.
Main Results:
- S1P significantly promoted corneal repair and increased nerve regeneration markers (NGF, BDNF, GDNF, p-ERK1/2).
- si-Spns2 treatment inhibited S1P's beneficial effects and exacerbated corneal injury.
- S1P enhanced axonal differentiation of trigeminal ganglion neurons, a process blocked by si-Spns2.
Conclusions:
- S1P promotes corneal trigeminal neuron differentiation and nerve repair by upregulating nerve growth factor.
- S1P represents a promising therapeutic agent for treating corneal injuries.
- Spns2 plays a critical role in mediating S1P's regenerative effects in the cornea.
