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-phos...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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De Gruyter
2022-10-01
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| Series: | Open Life Sciences |
| Subjects: | |
| Online Access: | https://doi.org/10.1515/biol-2022-0491 |
| _version_ | 1811246906064502784 |
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| author | Lin Chaoqun Li Weina Fan Xuezheng |
| author_facet | Lin Chaoqun Li Weina Fan Xuezheng |
| author_sort | Lin Chaoqun |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-12T15:01:22Z |
| format | Article |
| id | doaj.art-a85f3723ce274bddb749087e7342fb2b |
| institution | Directory Open Access Journal |
| issn | 2391-5412 |
| language | English |
| last_indexed | 2024-04-12T15:01:22Z |
| publishDate | 2022-10-01 |
| publisher | De Gruyter |
| record_format | Article |
| series | Open Life Sciences |
| spelling | doaj.art-a85f3723ce274bddb749087e7342fb2b2022-12-22T03:28:05ZengDe GruyterOpen Life Sciences2391-54122022-10-011711324133210.1515/biol-2022-0491S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse modelLin Chaoqun0Li Weina1Fan Xuezheng2Department of Neurosurgery, University of Chinese Academy of Sciences-Shenzhen Hospital (Guangming District), Shenzhen 518106, Guangdong, ChinaDepartment of Glaucoma and Cataract, Liuzhou Aier Eye Hospital, Affiliated Hospital of Aier Ophthalmology College of Central South University, 151 Liushi Road, Yufeng District, Liuzhou 545005, Guangxi, ChinaDepartment of Neurosurgery, University of Chinese Academy of Sciences-Shenzhen Hospital (Guangming District), Shenzhen 518106, Guangdong, ChinaCorneal 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.https://doi.org/10.1515/biol-2022-0491s1pcorneal trigeminal neuroncorneal nervespns2/erk1/2 signaling pathwaynerve growth factor |
| spellingShingle | Lin Chaoqun Li Weina Fan Xuezheng S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model Open Life Sciences s1p corneal trigeminal neuron corneal nerve spns2/erk1/2 signaling pathway nerve growth factor |
| title | S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model |
| title_full | S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model |
| title_fullStr | S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model |
| title_full_unstemmed | S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model |
| title_short | S1P promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model |
| title_sort | s1p promotes corneal trigeminal neuron differentiation and corneal nerve repair via upregulating nerve growth factor expression in a mouse model |
| topic | s1p corneal trigeminal neuron corneal nerve spns2/erk1/2 signaling pathway nerve growth factor |
| url | https://doi.org/10.1515/biol-2022-0491 |
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