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Publication : Inhibition of miR-665-3p Enhances Autophagy and Alleviates Inflammation in Fusarium solani-Induced Keratitis.

First Author  Guo Q Year  2021
Journal  Invest Ophthalmol Vis Sci Volume  62
Issue  1 Pages  24
PubMed ID  33481985 Mgi Jnum  J:301668
Mgi Id  MGI:6504072 Doi  10.1167/iovs.62.1.24
Citation  Guo Q, et al. (2021) Inhibition of miR-665-3p Enhances Autophagy and Alleviates Inflammation in Fusarium solani-Induced Keratitis. Invest Ophthalmol Vis Sci 62(1):24
abstractText  Purpose: Accumulated evidence has shown that microRNAs (miRNAs) are closely related with the regulation of autophagy, which plays vital roles in fungal keratitis (FK). Microarray data showed elevated expression of miR-665-3p in mouse corneal tissues after infection with Fusarium solani (F. solani). Here, we investigated the effect of miR-665-3p in regulating autophagy in experimental F. solani keratitis and determined the potential molecular mechanisms involved. Methods: In this article, we established an in vivo mouse model of FK and an in vitro model of corneal stromal cells by inoculating with F. solani. We divided them into the following six groups: control, chloroquine (CQ), rapamycin (Rapa), miR-665-3p antagomir (ant-665), miR-665-3p agomir (miR-665), and the negative control group (miR-NC). The levels of autophagy were detected by electron microscopy, Western blotting, and immunofluorescence. Then, we used a dual-luciferase reporter assay to determine the binding of miR-665-3p to the autophagy-related gene (ATG)5 3'UTR. Detection of IL-1beta protein levels and hematoxylin and eosin (H&E) staining of corneal tissues were used to observe the effect of miR-665-3p on inflammation in FK. Results: Here, we showed that inhibition of miR-665-3p expression in FK upregulated autophagy and alleviated inflammation. Nevertheless, the opposite results were found by overexpressing miR-665-3p. Additionally, ATG5 was a direct target gene for miR-665-3p. Conclusions: Together, our data demonstrated that miR-665-3p might be involved in F. solani keratitis of mice by regulating autophagic pathways and inflammation.
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