Objective and design

Diabetic retinopathy (DR) is one of the most serious microvascular complications of diabetes mellitus (DM). MicroRNAs (miRNAs) have been discovered to play a crucial role in DR, but the mechanisms underlying the effects of miR-301a-3p on DR are poorly understood. This paper was designed to explore the possible role of miR-301a-3p in DR.

Methods

The diabetic rat model was established by a single intraperitoneal injection of streptozotocin (STZ). The effects of miR-301a-3p on the biological functions of HRECs were determined through a series of experiments in vitro/vivo.

Results

The results revealed that interference with miR-301a-3p could decrease the expressions of inflammatory factors and apoptosis in the retinal tissue of DR. Furthermore, it can alleviate the oxidative stress in DR serum, reduce VEGF expression, increase endothelial cell marker expression, and inhibit (High Glucose) HG-induced apoptosis of HRECs. Six-transmembrane epithelial antigen of prostate 4 (STEAP4) was the target of miR-301a-3p. All the effects of miR-301a-3p in DR model were reversed by STEAP4 inhibitor.

Conclusion

miR-301a-3p promotes diabetic retinopathy via regulation of STEAP4. The findings in this study may provide a vital reference for the drug research and development in DR treatment.

中文翻译：

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MicroRNA-301a-3p 通过调节前列腺六跨膜上皮抗原促进糖尿病视网膜病变 4

 目的与设计

糖尿病视网膜病变（DR）是糖尿病（DM）最严重的微血管并发症之一。人们发现 MicroRNA (miRNA) 在 DR 中发挥着至关重要的作用，但 miR-301a-3p 对 DR 影响的机制尚不清楚。本文旨在探讨 miR-301a-3p 在 DR 中的可能作用。

 方法

通过单次腹腔注射链脲佐菌素（STZ）建立糖尿病大鼠模型。通过一系列体外/体内实验确定miR-301a-3p对HRECs生物学功能的影响.

 结果

结果表明，干扰miR-301a-3p可以减少DR视网膜组织中炎症因子的表达和细胞凋亡。此外，它还可以减轻 DR 血清中的氧化应激，降低 VEGF 表达，增加内皮细胞标志物表达，并抑制（高糖）HG 诱导的 HREC 凋亡。前列腺六跨膜上皮抗原 4 (STEAP4) 是 miR-301a-3p 的靶标。 STEAP4抑制剂逆转了miR-301a-3p在DR模型中的所有作用。

 结论

miR-301a-3p 通过调节 STEAP4 促进糖尿病视网膜病变。本研究结果可为DR治疗药物研发提供重要参考。