Journal
MOLECULAR THERAPY-NUCLEIC ACIDS
Volume 7, Issue -, Pages 71-80Publisher
CELL PRESS
DOI: 10.1016/j.omtn.2017.02.008
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Funding
- Fundamental Research Funds for the Central Universities [2016FZA7009]
- Zhejiang Provincial Natural Science Foundation of China [LY17H120001]
- Key Program of Natural Science Foundation of China [81130018]
- Program of National Natural Science Foundation of China [81371001]
- Program of National Natural Science Foundation [81428005]
- Project of National Clinical Key Discipline of the Chinese Ministry of Health, Zhejiang ProvinceKey Research and Development Program
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m-miR-184 (mutant miR-184, r.57c > u) appears in familial hereditary ocular diseases, including keratoconus, cataracts, EDICT (endothelial dystrophy, iris hypoplasia, congenital cataract, and stromal thinning) syndrome, severe keratoconus, and non-ectatic corneal thinning. The biological function of m-miR-184 in these ocular diseases remains unclear. With the emergence of high-throughput sequencing, it is now possible to discover many different biological components simultaneously. Using two different RNA libraries, we sequenced the complete transcriptome of HLE cells treated with miR-184, m-miR-184, and a negative control. Data were integrated in an effort to identify any novel gene affected by m-miR-184. Notably, we concluded that ALDH5A1 and GABRA3 were disordered by m-miR-184, which might lead to ocular disease. Moreover, circRNA (circular RNA) expression was highy random across miR-184, m-miR-184, and negative control treatment groups. The sequences of the circRNAs did reveal a particularly high level of ALU sequences. In summary, we provide a new avenue for understanding the role of m-miR-184 in ocular diseases.
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