z-logo
Premium
Identification of hsa‐mir‐34a, hsa‐mir‐124, and hsa‐mir‐204 as signatures for cataract
Author(s) -
Wei YingLi,
Sun Hao
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27741
Subject(s) - microrna , transcription factor , gene , biology , pathogenesis , computational biology , downregulation and upregulation , bioinformatics , genetics , immunology
Cataract, one of the common age‐related diseases that remains the leading cause of blindness worldwide. There have been studies pertaining to microRNA (miRNA) effects on cataract pathogenesis. However, the results were different from each other due to the influence of sequencing platform, sample selection, filter conditions, and so on. This study aims to explore the key miRNAs underlying the pathogenesis of cataract and find prevention and treatment methods. First, six representative cataract miRNA datasets are selected and the key miRNAs are determined. The target genes of these key miRNAs are predicted using the TargetScan software, and then, the functional enrichment and transcription factor binding analysis of these target genes are completed, respectively. Three signature miRNAs associated with cataract are finally identified. Among them, hsa‐mir‐34a seems to be significantly upregulated, while hsa‐mir‐124 and hsa‐mir‐204 are significantly downregulated. The target genes of the signature miRNAs are mainly enriched in hsa04015:Rap1 signaling pathway, hsa04142:lysosome, and hsa04360:axon guidance, indicating that these pathways may be the crucial metabolic pathways. To summarize, three key miRNAs related to cataract pathogenesis are identified, and the corresponding target genes and transcription factors are also analyzed. Moreover, the potential functions of the target genes are revealed. The results of this study may contribute to the targeted therapy of cataract through miRNAs.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here