Mechanism of Myopic Defocus or Atropine for Myopia Control: Different or Similar Ways?

Myopia is usually caused by excessive elongation of the eye during development. This condition is common worldwide. In clinical practice, the progression of myopia is commonly controlled through optical or drug measures, but the specific mechanisms underlying these two treatments remain unclear. To verify whether the effects of these two treatments on posterior-pole tissues are similar or different, we studied a set of common transcriptional changes in chicken models.

Chicks were divided into four groups, and they were given the intervention measures of plus-lens induction, minus-lens induction, minus-lens induction with atropine injection, and minus-lens induction with saline injection. Then, the genetic changes in each tissue at the posterior pole were detected, and the results of different genes were compared. A semiquantitative real-time polymerase chain reaction method was used to further study the visually induced changes in the transcription of potential candidate genes.

Based on RNA sequencing (RNA-seq) analysis of the transcriptome, we identified variations between the differentially expressed transcripts in three tissues from the two treatment groups. Through Kyoto Encyclopedia of Genes and Genomes enrichment analyses, eukaryotic protein translation elongation factor 1α2 (EEF1A2) was enriched in the "leishmaniasis" pathway in the choroid and showed increased expression in both the plus-lens induction and injection atropine groups. The expression levels of selected genes verified by quantitative real-time PCR were concordant with the RNA-seq data.

Overlapping differentially expressed mRNAs of only one-tenth could suggest a different mechanism of myopic defocus and intravitreal injection of atropine controlling myopia. EEF1A2 might play an important role in the choroid during the treatment of myopia.