Investigation of the molecular mechanisms underlying myotonic dystrophy types 1 and 2 cataracts using microRNA‑target gene networks
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- Published online on: July 21, 2017 https://doi.org/10.3892/mmr.2017.7059
- Pages: 3737-3744
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Copyright: © Shao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The purpose of the present study was to investigate the molecular mechanisms of myotonic dystrophy (DM) 1 and 2 cataracts using bioinformatics methods. A microarray dataset (E‑MEXP‑3365) downloaded from the Array Express database included lens epithelial samples of DM1 and DM2 cataract patients (n=3/group) and non‑DM lens epithelial samples as a control (n=4). Differentially expressed genes (DEGs) were identified between DM1 and control samples, and between DM2 and control samples. Pathway enrichment analyses were performed for the DEGs. Potential micro (mi)RNAs regulating these DEGs were predicted. An miRNA‑target gene network was constructed for DM1 and DM2. The study identified 223 DEGs in DM1, and 303 DEGs in DM2. DM1 and DM2 shared 172 DEGs. The DEGs in DM1 were enriched with calcium, Wnt and axon guidance signaling pathways. The DEGs in DM2 were linked by adherens junction signaling pathways. miRNA (miR)‑197, miR‑29b and miR‑29c were included in the network modules of DM1. miR‑197, miR‑29c and miR‑29a were involved in the network modules of DM2. It is therefore hypothesized that these signaling pathways and miRNAs underlie DM1 and DM2 cataracts, and may represent potential therapeutic targets for the treatment of this disorder.
