4.7 Article

Inhibitory effect of miR-138-5p on choroidal fibrosis in lens-induced myopia guinea pigs via suppressing the HIF-1 alpha signaling pathway

Journal

BIOCHEMICAL PHARMACOLOGY
Volume 211, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.bcp.2023.115517

Keywords

HIF-1 alpha signaling pathway; Lens-induced myopia; Choroidal fibrosis; TGF-beta 1; Collagen I; alpha-SMA

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This study aimed to investigate the effect of miR-138-5p on choroidal fibrosis in myopic guinea pigs via regulating the HIF-1 alpha signaling pathway. The results showed that miR-138-5p can efficiently decrease the refraction and ocular length, and ameliorate the choroidal fibrosis of the experimental myopic guinea pigs through inhibiting the HIF-1 alpha signaling pathway. These findings provide new insight into controlling myopic development using microRNAs in clinical practice.
Myopia is one of the most common eye diseases in children and adolescents worldwide. Currently, there is no effective treatment in clinical practice. Ocular tissue fibrosis is involved in the development of myopia and this study aimed to investigate the effect of miR-138-5p on choroidal fibrosis in myopic guinea pigs via regulating the HIF-1 alpha signaling pathway. First, guinea pigs were randomly divided into a normal control (NC) group, a lensinduced myopia (LIM) group, a LIM + miR-138-5p-carried Lentivirus treatment (LV) group, and a LIM + miR138-5p-Vector treatment (VECTOR) group. All animals were induced experimental myopia with a -6.0 diopter lens except those in the NC group. Meanwhile, animals in the LV group were supplemented with 5 mu l of miR-138-5p-carried Lentivirus, while those in the VECTOR group were only supplemented with the same volume of miR138-5p-Vector. After myopia induction for 2 and 4 weeks, the refractive status and other ocular parameters of the guinea pigs were measured. Further, the expression of hypoxia-inducible factor (HIF)-1 alpha, transforming growth factor (TGF)-beta, collagen I, hydroxyproline (HYP), interleukin 1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), and alpha-smooth muscle actin (alpha-SMA) in choroidal tissues was investigated. Results showed that the refraction and axial length of the experimental myopic guinea pigs increased, and choroid fibrosis aggravated after experimental myopic induction. miR-138-5p can efficiently decrease the refraction and ocular length, and ameliorate the choroidal fibrosis of the experimental myopic guinea pigs via downregulating the fibrosis-related TGF-beta 1, collagen I, HYP, IL-1 beta, TNF-alpha, and alpha-SMA expression through inhibiting the HIF-1 alpha signaling pathway. Our results provide new insight into controlling myopic development using microRNAs in clinical practice.

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