MiR-181a-5p may regulate cell proliferation and autophagy in myopia and the associated retinopathy.

The mechanism of myopia and the associated retinopathy remains unclear, and dysregulated microRNAs (miRNAs) are implicated in this disease. In this research, we purposed to find out the regulatory function that miRNAs play in myopia and the associated retinopathy. We first performed miRNA microarray analysis in a lens-induced myopia mouse model and found that miR-9-5p, miR-96-5p, miR-182-5p, miR-183-5p, and miR-181a-5p were elevated in the myopic retina. Then, we examined the functions and regulatory mechanisms of miR-181a-5p utilizing the human retinal pigment epithelium (RPE) cell line ARPE-19 by overexpressing miR-181a-5p. RNA sequencing (RNA-Seq) and qRT-PCR analysis were employed to identify differentially expressed genes after transfection. The qRT‒PCR outcomes, immunoblotting, and immunofluorescence indicated that the SGSH expression was significantly hindered through miR-181a-5p overexpression. MiR-181a-5p overexpression has the ability to elevate RPE cell proliferation and induce autophagy by targeting SGSH. We validated the negative influence of miR-181a-5p on the SGSH expression through luciferase reporter assays, which demonstrated its ability to target the 3' untranslated region of SGSH. The reversal of implications of miR-181a-5p overexpression was achieved through SGSH upregulation. We provided novel perspectives into the miR-181a-5p function in regulating myopia development and may serve as a target for therapy and molecular biomarker for myopia.

The national, regional, and global impact of glaucoma as reported in the 2019 Global Burden of Disease Study.

Introduction: We investigated the disability-adjusted life years (DALYs) of glaucoma. Methods: The estimated annual percentage change (EAPC) was measured to assess trends in the age-standardized DALY rate from 1990 to 2019. Results: The global age-standardized DALY rate of glaucoma decreased with an EAPC of -1.00. The age-standardized DALY rate decreased least in high-SDI regions. Eastern sub-Saharan Africa had highest age-standardized DALY rate in 2019. At the national level, Mali had the highest age-standardized DALY rate in 2019. Conclusions: Although the global burden of glaucoma has decreased, the burden remain high in regions with low SDI values and in sub-Saharan Africa.

[Insulin-like growth factor 1 (IGF-1) promotes phagocytic activity of mouse BV-2 microglial cells via activating PI3K/AKT signaling pathway].

Objective To investigate the effect of insulin-like growth factor 1 (IGF-1) on the phagocytic activity of mouse BV-2 microglial cells. Methods Western blotting was performed to detect the protein levels of IGF-1 and IGF-1 receptor (IGF-1R) in the murine brain after the establishment of acute central nervous system inflammation models by intraperitoneal lipopolysaccharide (LPS) injection (10 mg/kg). The protein level of IGF-1R on BV-2 microglial cells that had been stimulated by 500 ng/mL LPS for 4, 12 and 24 hours was measured by Western blotting. To assess the phagocytic activity of microglial cells in response to IGF-1, BV-2 microglial cells were stimulated by IGF-1 at different concentrations for 24 hours after pretreated with or without wortmannin (PI3K/AKT signaling pathway blocker), and then incubated with fluorescent microbeads for 2 hours followed by measurement of phagocytosis of the fluorescent microbeads by flow cytometry. After treatment of IGF-1 (50 ng/mL), p-AKT and AKT signaling pathways in the BV-2 microglial cells were detected by Western blotting. Results Intraperitoneal LPS injection caused increased levels of IGF-1 and IGF-1R in the mouse brain. LPS upregulated the protein expression of IGF-1R on BV-2 microglial cells. The activity of BV-2 microglial cells to phagocytose fluorescent microbeads gradually increased with IGF-1 concentration rising and peaked in the IGF-1 treatment at 50 ng/mL, and gradually decreased thereafter. And IGF-1 induced the phosphorylation of AKT in BV-2 microglial cells. However, after the PI3K/AKT signaling pathway was blocked via wortmannin, the effect of IGF-1 on the activity of BV-2 microglial cells to phagocytose fluorescent microbeads was significantly alleviated. Conclusion IGF-1 can promote phagocytic activity of BV-2 cells via activating PI3K/AKT signaling pathway, which suggests a potential role of IGF-1 in regulating the cerebral inflammation.