miR-29a/b cluster suppresses high glucose-induced endothelial-mesenchymal transition in human retinal microvascular endothelial cells by targeting Notch2.

Several studies have previously reported that endothelial cells contributed to pathological fibrosis in proliferative diabetic retinopathy (PDR) through endothelial-mesenchymal transition (EndMT); however, the precise mechanism of this interaction has not been completely elucidated. The present study investigated the expression of microRNA (miR)-29a/b cluster in human retinal microvascular endothelial cells (HRMECs) and examined its functional role in high glucose (HG)-induced EndMT. HRMECs were exposed to glucose at concentrations of 5, 15, 30 and 50 mM for 7 days and reverse transcription-quantitative polymerase chain reaction, western blotting and immunofluorescence were conducted to determine the expression of genes associated with miR-29a/b and EndMT.

Correlation analysis for school-age children's height and refractive errors.

Background: During the rapid physical and mental development, school-age children, who are beginning the learning phase, have an increasingly heavy burden on their eyes.

Objectives: The aim of this study was to analyze the association of refractive errors with body height in children aged 7-14 years.

Material And Methods: A total of 1,696 children aged 7-14 years were consecutively enrolled.

Downregulation of MicroRNA 29a/b exacerbated diabetic retinopathy by impairing the function of Müller cells via Forkhead box protein O4.

Background: Diabetic retinopathy is a neurological disease, which can lead to blindness in severe cases. The pathogenesis underlying diabetic retinopathy is unclear. The aim of this study was to explore the role of dysregulated microRNA 29a/b in the onset and progression of diabetic retinopathy.

Long non-coding RNA MIAT acts as a biomarker in diabetic retinopathy by absorbing and regulating cell apoptosis.

Diabetic retinopathy (DR) is a complication of diabetes mellitus (DM) and is the leading cause of vision loss globally. However, the pathogenic mechanism and clinical therapy still needs further improvement. The biologic significance of myocardial infarction associated transcript (MIAT) in DR remains unknown.