Knockdown of FBXL19-AS1 exerts a protective effect on Human retinal endothelial cells treated with high glucose by targeting miR-200c-3p.

Objective

Proliferative diabetic retinopathy (PDR) is a leading cause of blindness. FBXL19-AS1 is highly expressed in the retinas of PDR patients. This study aims to investigate its diagnostic value in PDR and its potential regulatory mechanisms.

Methods

A total of 102 patients with PDR were enrolled. RT-qPCR was used to detect the levels of FBXL19-AS1 and miR-200c-3p in patients with PDR and in HREC cells treated with high glucose (HG). ROC analysis evaluated their diagnostic value. Cell proliferation was assessed using the CCK-8 assay. Cell migration was evaluated via Transwell assays. Apoptosis was analyzed by flow cytometry. Concurrently, RT-qPCR measured cellular expression levels of VEGF, Ang-2, Bax, and Bcl-2. DLR validated the binding relationship between FBXL19-AS1 and miR-200c-3p.

Results

In serum samples from patients with PDR and in HREC cells from the HG group, FBXL19-AS1 expression was upregulated and demonstrated promising diagnostic value. HREC cells in the HG group exhibited abnormal proliferation and migration, with elevated VEGF levels. Following FBXL19-AS1 inhibition, miR-200c-3p was upregulated due to its targeted binding to FBXL19-AS1. Abnormal cell proliferation and migration were suppressed, apoptosis rates increased, and VEGF and Ang-2 expression decreased. However, these improvements were significantly reversed upon inhibition of miR-200c-3p levels.

Conclusion

FBXL19-AS1 regulates the proliferation, migration, and apoptosis of HRECs by sponging miR-200c-3p, thereby participating in the microvascular lesion process of PDR. This provides a new perspective for understanding the pathogenesis of PDR.