[Gene expression profiles of myopic mouse scleral fibroblasts: a bioinformatics analysis based on single-cell RNA sequencing].

OBJECTIVE

To investigate the changes in gene expression profiles of mouse scleral fibroblasts after myopia using single-cell RNA sequencing technology and explore the mechanism of dysfunction of the scleral fibroblasts in myopia.

METHODS

Normal healthy C57BL/6J mice were randomly divided into negative control group and myopia model group (n=6), and in the latter group, form deprivation myopia was induced in the right eye using translucent goggles. Single cell capture was performed in the right eye to obtain the scleral fibroblasts for RNA sequencing. The differentially expressed genes (DEGs) were screened and GO and KEGG analyses were carried out for functionally significant enrichment analysis.

RESULTS

Comparison of the gene expression profiles identified a total of 169 DEGs between the myopia model group and the negative control group (P>0.05), including 112 up-regulated and 57 down-regulated genes. GO function analysis showed that the DEGs were involved in leukocyte aggregation, differentiation and adhesion and other inflammation-related terms; ATP metabolism and binding, redox process, oxidative stress response, oxidative phosphorylation and other GO terms related to hypoxia; protein folding, protein transport, negative regulation of protein metabolism, endoplasmic reticulum (ER), ER cavity, ER stress and other biological processes related to protein and ER stress. KEGG analysis analysis showed that the significantly enriched pathways of the DEGs involved mainly the TCA cycle, oxidative phosphorylation, PPAR signaling, oxidative phosphorylation and other pathways related to hypoxia; MAPK signaling pathway related to inflammation; leukocyte transendothelial transport; and protein-related Parkinson's disease, Huntington's disease, protein digestion and absorption pathways.

CONCLUSION

The dysfunction of the scleral fibroblasts occurs in myopia through complex mechanisms involving inflammation, hypoxia, protein regulation, and ER stress-related gene expression and pathway regulation.