Silencing of miR-20b-5p Exerts Inhibitory Effect on Diabetic Retinopathy via Inactivation of THBS1 Gene Induced...

Area of Science:

• Ophthalmology
• Molecular Biology
• Genetics

Background:

• Diabetic retinopathy (DR) is a severe complication of diabetes, yet its molecular mechanisms remain poorly understood.
• MicroRNA-20b-5p (miR-20b-5p) is identified as upregulated in DR, necessitating further investigation into its role.
• Current research gaps hinder the development of effective clinical treatments for DR.

Purpose of the Study:

• To confirm the involvement of miR-20b-5p in the pathogenesis of diabetic retinopathy.
• To elucidate the underlying molecular mechanism by which miR-20b-5p influences DR.
• To identify potential therapeutic targets for managing DR.

Main Methods:

• Differential gene expression analysis using microarray and bioinformatics.
• Establishment of a rat model of diabetic retinopathy.
• Manipulation of miR-20b-5p and THBS1 expression using inhibitors, mimics, and siRNA.
• Assessment of the VEGF/PI3K/Akt signaling pathway.
• Evaluation of endothelial cell apoptosis, proliferation, and tube formation.

Main Results:

• Overexpression of miR-20b-5p and decreased THBS1 were observed in retinal tissues of DR rats, mediated by the VEGF/PI3K/Akt cascade.
• THBS1 was validated as a direct target gene of miR-20b-5p.
• Upregulation of miR-20b-5p or knockdown of THBS1 promoted endothelial cell proliferation and tube formation while inhibiting apoptosis.

Conclusions:

• Silencing miR-20b-5p effectively inhibits vascular endothelial cell proliferation and tube formation in DR.
• Downregulation of miR-20b-5p leads to THBS1 upregulation, impacting the VEGF/PI3K/Akt pathway.
• Targeting miR-20b-5p presents a promising therapeutic strategy for diabetic retinopathy.