Effects of microRNA-29a on retinopathy of prematurity by targeting AGT in a mouse model.

BACKGROUND

This study aimed to explore the effects of microRNA-29a (miR-29a) on retinopathy of prematurity (ROP) by targeting angiotensinogen (AGT) expression in a mouse model.

METHODS

Ninety-six C57BL/6J mice were selected and divided into the normal control group (n = 12) and the oxygen-induced retinopathy (OIR) group (n = 84). All the mice in the OIR group were assigned to the following seven groups (12 mice in each group): the blank, miR-29a mimics, miR-29a inhibitors, empty plasmid, miR-29a mimics + si-AGT, miR-29a inhibitors + si-AGT and si-AGT groups. ADPase histochemical staining was conducted to detect the morphology of retinal neovascularization. H&E staining was performed to quantify retinal neovascularization. The qRT-PCR assay was applied to detect the expression levels of miR-29a and the mRNA. Western blotting was used to detect the protein expressions of AGT, vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), angiotensin (ANG) and angiotensin II (AngII).

RESULTS

Compared with the normal control group, miR-29a expression decreased, while the mRNA expression and the protein expression levels of AGT, VEGF, HGF, ANG and AngII increased, and retinal vascular density and neovascularization also increased in the OIR group. In the OIR group, compared with the blank, empty plasmid, miR-29a inhibitors and miR-29a inhibitors + si-AGT groups, miR-29a expression increased, while the mRNA expression and protein expression levels of AGT, VEGF, HGF, ANG and AngII decreased, and retinal vascular density and neovascularization also decreased in the miR-29a mimics, miR-29a mimics + si-AGT and si-AGT groups.

CONCLUSION

MiR-29a could inhibit retinal neovascularization to prevent the development and progression of ROP by down-regulating AGT.