MiR-29 regulates retinopathy in diabetic mice via the AMPK signaling pathway.

Abstract

This work aims to study the influence of micro-ribonucleic acid (miR)-29 on the retinopathy in diabetic mice via the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway. A total of 24 C57BL/6 mice were randomly divided into normal group (n=12) and model group (n=12). Mice in the normal group were given to normal diet, and those in the model group were prepared for establishing diabetes mouse model. After animal procedures, electroretinogram was performed to detect the latent period and amplitude of b-wave. The expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected via immunohistochemistry. The protein levels of the phosphorylated AMPK (p-AMPK) and phosphorylated mammalian target of rapamycin (p-mTOR) were determined using Western blotting. Moreover, miR-29 expression and cell apoptosis were detected via quantitative Polymerase Chain Reaction (qPCR) and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL), respectively. Compared with those in the normal group, the latent period prolonged and amplitude of b-wave decreased in the model group (p<0.05). Immunohistochemistry showed that compared with normal group, mice in the model group exhibited increased Bax expression and decreased Bcl-2 expression (p<0.05). The Western blotting analysis showed that the protein levels of p-AMPK decreased and p-mTOR increased in the model group compared with those in the normal group (p<0.05). The qPCR revealed that compared with the normal group, the model group had notably decreased miR-29 expression (p<0.05). TUNEL detection displayed that the apoptotic rate was remarkably elevated in the model group compared with that in the normal group (p<0.05). Inhibition of miR-17-5p up-regulates the expression of VEGF-A and GDNF in MSCs, and promotes the repair of spinal cord injury by MSCs.