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Updated: Jul 6, 2025
An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse
Published on: April 7, 2014
Exploring Corneal Neovascularization: An Integrated Approach Using Transcriptomics and Proteomics in an Alkali Burn
Wei Wang1, Manli Deng1, Min Li1
1Department of Ophthalmology, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.
Purpose:
Corneal neovascularization (CNV) impairs corneal transparency and visual acuity. The study aims to deepen our understanding of the molecules involved in CNV induced by alkali burns, facilitate a better grasp of CNV mechanisms, and uncover potential therapeutic targets.
Methods:
Eighty-four mice were selected for establishing CNV models via alkali burns. On days 3, 7, and 14 after the burns, corneal observations and histological investigations were conducted. An integrated analysis of RNA sequencing (RNA-seq)-based transcriptomics and label-free quantitative proteomics was performed in both normal and burned corneas. Bioinformatics approaches, encompassing Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, were applied to discern differentially expressed genes (DEGs) and crucial signaling pathways. Four potentially CNV-related genes were validated using quantitative real-time PCR (qRT-PCR) and Western blot.
Results:
Significant CNV was observed on the seventh day. Forty-one genes were differentially expressed in neovascularized corneas, with 15 upregulated and 26 downregulated at both mRNA and protein levels. Bioinformatics analysis revealed that these DEGs participated in diverse biological processes, encompassing retinol and retinoic acid metabolism, neutrophil chemotaxis, and actin filament assembly, along with significant enrichment pathways like cytochrome P450, tyrosine, and phenylalanine metabolism. The upregulation of lymphocyte cytosolic protein 1 (LCP1) and cysteine and glycine-rich protein 2 (CSRP2) genes and the downregulation of transglutaminase 2 (TGM2) and transforming growth factor-beta-induced (TGFBI) genes were confirmed.
Conclusions:
We analyzed gene expression differences in mouse corneas 7 days after alkali burns, finding 41 genes with altered expression. The exact role of these genes in CNV is not fully understood, but exploring angiogenesis-related molecules offers potential for CNV treatment or prevention.
Insights
Alkali burns cause corneal neovascularization (CNV) by altering 41 gene expressions. Understanding these angiogenesis-related molecules may lead to new treatments for CNV, improving vision.
Area of Science:
- Ophthalmology
- Molecular Biology
- Genomics
Background:
- Corneal neovascularization (CNV) is a significant cause of vision impairment.
- Alkali burns are a common cause of corneal injury and subsequent CNV.
- Identifying molecular mechanisms underlying CNV is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the molecular changes in corneal neovascularization (CNV) induced by alkali burns.
- To understand the mechanisms driving CNV development.
- To identify potential therapeutic targets for CNV.
Main Methods:
- Corneal neovascularization (CNV) models were established in mice using alkali burns.
- Integrated transcriptomic (RNA-seq) and proteomic analyses were performed on normal and burned corneas.
- Bioinformatics approaches (GO, KEGG) identified differentially expressed genes (DEGs) and signaling pathways. Validation was done using qRT-PCR and Western blot.
Main Results:
- Significant CNV was observed by day 7 post-burn.
- Forty-one genes showed differential expression (15 upregulated, 26 downregulated) at both mRNA and protein levels.
- DEGs were involved in retinol metabolism, neutrophil chemotaxis, and actin assembly; key pathways included cytochrome P450 and amino acid metabolism. LCP1 and CSRP2 were upregulated; TGM2 and TGFBI were downregulated.
Conclusions:
- Gene expression analysis revealed 41 altered genes in mouse corneas 7 days after alkali burns.
- While the precise role of these genes in CNV requires further investigation, they represent potential targets for CNV treatment or prevention.
- Exploring angiogenesis-related molecules identified in this study may offer new therapeutic strategies for corneal neovascularization.
