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DOI 10.1002/jcla.23571

Медицинская библиотека · Journal of clinical laboratory analysis · 2020

The expression of miRNA-146a-5p and its mechanism of treating dry eye syndrome.

Yin Liang, Zhang Mingxue, He Tiangeng, Chen Song

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Аннотация

OBJECTIVE

Dry eye syndrome in which tear fluid quality or abnormality, or kinetic abnormality is caused by various reasons, resulting in decreased tear film stability. In recent years, more and more results from the studies indicate that miRNA alterations are involved in dry eye syndrome. And miRNA-146a-5p is a key regulator to regulate the inflammatory response. In this paper, we demonstrated whether miRNA-146a-5p could cure dry eye syndrome by regulating target genes based on network analysis.

METHODS

In current study, we collected the blood of patients with dry eye disease served as a model group; the blood of healthy people was served as control group. The expression of miRNA-146a-5p in the patients was detected by RT-PCR, the genes controlled by miRNA-146a-5p were predicted by TargetScan, miRDB, miRWalk, and PicTar databases, and the genes regulated by miRNA-146a-5p which relative with dry eye disease were selected by drawing Venn diagram.

RESULTS

The comparison of the general information between patients and healthy people was no significant difference, and it indicated that the two groups were comparable. The results of databases showed that IRAK1 was one of the target genes regulated by miRNA-146a-5p, and it is related to dry eye disease. The expression of miRNA-146a-5p was negatively related to IRAK1 mRNA and protein, while IRAK1 had a positive correlation with IL-6, TNF-α, and CBP proteins.

CONCLUSION

These results emphasized that miRNA-146a-5p could inhibit the expression of IRAK1, IL-6, TNF-α, and CBP to help reduce the inflammatory response in dry eye syndrome.

Для цитирования: Yin Liang, Zhang Mingxue, He Tiangeng, Chen Song. The expression of miRNA-146a-5p and its mechanism of treating dry eye syndrome.. Journal of clinical laboratory analysis. 2020. DOI: 10.1002/jcla.23571.

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