Abstract
Background: Diabetic retinopathy (DR) is the most important manifestation of diabetic microangiopathy. MicroRNAs (miRNAs), members of non-coding RNAs, have been frequently reported to regulate various diseases including DR. MiR-124-3p is involved in DR based on bioinformatics. The current study aimed to investigate the role of miR-124-3p in high glucose (HG)-treated human retinal microvascular endothelial cells (HRMECs), an in vitro model of DR.Methods: Bioinformatics analysis was applied to reveal the targets downstream miR-124-3p. A series of assays including CCK-8, luciferase reporter, western blot, and tube formation assays were used to explore the function and mechanism of miR-124-3p in HG-stimulated HRMECs.Results: We found out that miR-124-3p was downregulated in HG-stimulated HRMECs. Functionally, miR-124-3p overexpression restrained the HG-induced cell injury of HRMECs. Mechanistically, we predicted 5 potential target mRNAs of miR-124-3p. G3BP stress granule assembly factor 2 (G3BP2) was validated to bind with miR-124-3p. Rescue assays showed that miR-124-3p suppressed cell injury of HG-stimulated HRMECs through G3BP2. In addition, miR-124-3p regulated the p38MAPK signaling pathway by G3BP2, and G3BP2 promoted injury of HG-treated HRMECs through the activation of the p38MAPK signaling pathway.Conclusion: MiR-124-3p suppressed the dysfunctions of HG-treated HRMECs by targeting G3BP2 and activating the p38MAPK signaling. This new discovery provided a potential biomarker for DR treatment.
Highlights
Diabetic retinopathy (DR) is a common microvascular complication of diabetes (Cheung et al, 2010; Henriques et al, 2015; Diallo et al, 2019)
The results demonstrated that the viability of human retinal microvascular endothelial cells (HRMECs) was enhanced by high glucose (HG) treatment for 24 h, and 30 mM HG achieved the best effects (Figure 1A)
We miR-124-3p in Diabetic Retinopathy found that miR-155-5p, miR-122-5p, miR-223-3p, miR-125b5p were all downregulated in HG-treated HRMECs, while expression of miR-1-3p showed no significant difference between control and HG groups (Supplementary Figure 1A)
Summary
Diabetic retinopathy (DR) is a common microvascular complication of diabetes (Cheung et al, 2010; Henriques et al, 2015; Diallo et al, 2019). Features of DR include blood-retina barrier (BRB) breakdown, capillary acellularity and pericyte loss and it has been confirmed that the main factor contributing to the progression of DR is chronic hyperglycemia In the early stage of DR, human retinal microvascular endothelial cells (HRMECs), components of the BRB, are impaired by the adverse impact of high glucose (HG), resulting in BRB dysfunction and accelerating DR progression (Strauss, 2005; Miyamoto et al, 2007). HRMEC was employed as an in vitro model of DR in this study. The current study aimed to investigate the role of miR-1243p in high glucose (HG)-treated human retinal microvascular endothelial cells (HRMECs), an in vitro model of DR
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