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Published on: April 3, 2016
Alterations in N6-Methyladenosine (m6A) Modification of mRNA in the Sclera of Form-Deprived Myopic Guinea Pig
Jie Wang1, Lingling Ba1, Jiantao Ren1,2
1Tianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, China.
Purpose:
This study aimed to provide direct evidence of the potential role of N6-methyladenosine (m6A) modification in the progression of myopia. We focused on identifying genes that may be involved in scleral remodeling through m6A regulation in myopia.
Methods:
We utilized m6A methylation immunoprecipitation sequencing (MeRIP-seq) alongside RNA sequencing (RNA-seq) to investigate the levels of m6A modification and mRNA expression in the scleras of form-deprived myopic (FDM) guinea pigs. Subsequent bioinformatics analysis was performed to identify the enriched pathways and genes associated with m6A modification.
Results:
Bioinformatic analyses indicated that hypermethylated mRNAs were predominantly associated with the calcium signaling pathway and may participate in extracellular matrix (ECM) remodeling. Through integrated analysis of MeRIP-seq and RNA-seq data, it was found that more than half of the differentially expressed modified genes (DEGs) exhibiting increased mRNA levels also showed an upregulation of m6A modification levels. These genes may play significant roles in the process of myopic scleral remodeling in response to elevated levels of methyltransferase METTL14.
Conclusion:
This study highlights the role of m6A methylation, mediated by METTL14, in the regulating of key genes involved in calcium signaling and ECM remodeling during myopia progression. These findings suggest that targeting m6A modifications may could offer new therapeutic strategies for the treatment of myopia.
Insights
N6-methyladenosine (m6A) modification, regulated by METTL14, plays a key role in myopia progression by influencing calcium signaling and extracellular matrix remodeling in the sclera. Targeting m6A may offer new myopia treatments.
Area of Science:
- Ophthalmology and Molecular Biology
- Epigenetics and Gene Regulation
Background:
- Myopia, a global vision impairment, involves scleral remodeling.
- The role of epitranscriptomic modifications like N6-methyladenosine (m6A) in myopia is not fully understood.
Purpose of the Study:
- To investigate the direct evidence of m6A modification's role in myopia progression.
- To identify genes involved in scleral remodeling regulated by m6A in myopia.
Main Methods:
- Utilized m6A methylation immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) in form-deprived myopic (FDM) guinea pig scleras.
- Performed bioinformatics analysis to identify enriched pathways and genes associated with m6A modification.
Main Results:
- Hypermethylated mRNAs were linked to calcium signaling and extracellular matrix (ECM) remodeling.
- Over half of differentially expressed genes with increased mRNA levels showed upregulated m6A modification.
- Upregulated m6A modification and gene expression correlated with METTL14 levels in myopic scleras.
Conclusions:
- m6A methylation, mediated by METTL14, regulates key genes in calcium signaling and ECM remodeling during myopia progression.
- Targeting m6A modifications presents potential therapeutic strategies for myopia treatment.
