Possible role of miR-204 in optic nerve injury through the regulation of GAP-43.

Optic nerve injury is a common disease. The present study aimed to examine the possible role of microRNA‑204 (miR‑204) in optic nerve injury through the regulation of growth‑associated protein-43 (GAP‑43). Initially, optic nerve injury models were established in Sprague‑Dawley (SD) rats, and the function of miR‑204 was either enhanced or inhibited through injection of miR‑204 mimic and inhibitor, respectively. Subsequently, the mRNA and protein levels of miR‑204, GAP‑43, toll‑like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor‑κB (NF‑κB) were examined in retinal tissues using reverse transcription‑quantitative polymerase chain reaction and western blot analyses. The apoptosis of retinal tissue cells was also detected using a terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay. There was a significant increase in the level of miR‑204 in retinal blood vessels of the model SD rats, compared with that in the normal SD rats (P<0.05), and the expression of GAP‑43 was significantly decreased (P<0.05). The results confirmed that the expression of GAP‑43 was significantly reduced, compared with that in the normal control group when the rats were treated with miR‑204 mimic (P<0.05), which was similar to the result in the model group. By contrast, its expression of GAP‑43 was significantly increased when treated with the miR‑204 inhibitor (P<0.05). Compared with the normal control group, the expression levels of TLR4, MyD88 and NF‑κB were significantly increased in the miR‑204 mimic group and model group (P<0.05), whereas the same three factors in the miR‑204 inhibitor group were effectively inhibited, compared with those in the model group, and showed similar results to the normal control group. The apoptotic rates of retinal cells in the miR‑204 mimic group and model group were significantly increased, compared with that in the normal control group (P<0.05), whereas miR‑204 inhibitor effectively reversed the effects on apoptotic rate observed in the model group, showing similar results to those in the normal control group. Taken together, miR‑204 promoted the apoptosis of retinal cells through inhibiting GAP‑43, providing theoretical guidance for the function of GAP‑43 in retinal injury.