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Screening of potential target genes for cataract by analyzing mRNA expression profile of mouse Hsf4-null lens
Wenjuan Zhao1,2, Wenqing Zhao3, Jun Zhao4
1Department of Ophthalmology, Qilu Hospital of Shandong University, Wenhuaxi Road 107, Jinan, Shandong, 250012, China. WenjuanZhaooa@163.com.
Background:
Hsf4 is closely related to the development of cataract. However, the molecular mechanisms remain unknown. This study aimed to explore the molecular mechanisms that how Hsf4 mutations influence development of lens and thus lead to cataract in mouse.
Methods:
The mRNA expression profile of mouse tissue samples from Hsf4-null and wile-type lenses was downloaded from Gene Expression Omnibus database. Then the LIMMA package was used to screen differentially expressed genes (DEGs) and DAVID was applied to identify the significantly enriched Gene Ontology (GO) categories for DEGs. Furthermore, the protein-protein interaction (PPI) network of DEGs was constructed using Cytoscape and the key modules were selected from the PPI network based on the MCODE analysis.
Results:
A total of 216 DEGs were screened, including 51 up- and 165 down-regulated genes. Meanwhile, nine GO terms were obtained, and DEGs such as SGK1, CRY2 and REV1 were enriched in response to DNA damage stimulus. Furthermore, 89 DEGs and 99 gene pairs were mapped into the PPI network and Ubc was the hob node. Two key modules, which contained the genes (e.g. Ubc, Egr1, Ptgs2, Hmox1, Cd44, Btg2, Cyr61 and Fos) were related to response to DNA damage stimulus.
Conclusions:
The deletion of Hsf4 affects the expression of many genes, such as Ubc, Ptgs2, Egr1 and Fos. These genes may be involved in the development of cataract and could be used as therapeutic targets for cataract.
Insights
Hsf4 gene deletion impacts lens development and cataract formation by altering gene expression. Identified genes like Ubc and Ptgs2 may serve as novel therapeutic targets for cataract treatment.
Area of Science:
- Genetics
- Ophthalmology
- Molecular Biology
Background:
- Hereditary cataracts are linked to Hsf4 gene mutations.
- The precise molecular mechanisms underlying Hsf4's role in cataractogenesis are not fully understood.
Purpose of the Study:
- To investigate the molecular mechanisms by which Hsf4 mutations influence lens development and lead to cataracts in mice.
Main Methods:
- Differential gene expression analysis of Hsf4-null and wild-type mouse lenses using Gene Expression Omnibus data.
- Identification of significantly enriched Gene Ontology (GO) categories for differentially expressed genes (DEGs) via DAVID.
- Construction and analysis of a protein-protein interaction (PPI) network for DEGs using Cytoscape and MCODE.
Main Results:
- 216 DEGs were identified, with 51 upregulated and 165 downregulated.
- Nine GO terms were enriched, notably involving response to DNA damage stimulus (e.g., SGK1, CRY2, REV1).
- A PPI network highlighted Ubc as a hub node, with key modules related to DNA damage response.
Conclusions:
- Hsf4 deletion significantly alters the expression of numerous genes, including Ubc, Ptgs2, Egr1, and Fos.
- These affected genes are implicated in cataract development.
- The identified genes represent potential therapeutic targets for managing cataracts.
