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The following is a summary of “miR-16-5p Regulates Proliferation and Apoptosis in High Glucose–Treated Human Retinal Microvascular Endothelial Cells by Targeting VEGFA and TGFBR1,” published in the March 2025 issue of Journal of Ophthalmology by Zhao et al. 

Diabetic retinopathy (DR), a leading reason of vision loss in middle-aged and elderly individuals, involves miRNAs in its progression.  

Researchers conducted a retrospective study to analyze the effects of miR-16-5p on high glucose (HG)–stimulated human retinal microvascular endothelial cells (HRECs) by regulating vascular endothelial growth factor A (VEGFA) and transforming growth factor beta receptor 1 (TGFBR1).  

They exposed HRECs to HG at 5 mM, 10 mM, 20 mM, and 30 mM to establish a DR cell model. Real-time quantitative polymerase chain reaction (RT-qPCR) measured miR-16-5p and messenger RNA (mRNA) expression of VEGFA and TGFBR1. Western blot assessed VEGFA and TGFBR1 protein levels. The 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide assay evaluated cell proliferation. Flow cytometry with Annexin V-FITC/PI double staining determined the apoptosis ratio. The dual-luciferase assay confirmed the target relationship between miR-16-5p and VEGFA and TGFBR1.  

The results showed that miR-16-5p expression decreased in HG-treated HRECs, while VEGFA and TGFBR1 were upregulated. Knockdown of miR-16-5p elevated VEGFA and TGFBR1 mRNA and protein levels, increased cell proliferation by 35%, and reduced apoptosis by 28% in HG-treated HRECs. Inhibition of VEGFA and TGFBR1 reversed the effects of miR-16-5p knockdown. Dual-luciferase reporter assay confirmed that VEGFA and TGFBR1 were direct targets of miR-16-5p (P <0.05).  

Investigators concluded that the knockdown of miR-16-5p improved the proliferation and impeded the apoptosis of HRECs by upregulating the expression of VEGFA and TGFBR1. 

Source: onlinelibrary.wiley.com/doi/10.1155/joph/3082206