The role of microRNAs in corneal neovascularization and its relation to VEGF.

PURPOSE

This study aimed to investigate the changes in the level of associated with Vascular Endothelial Growth Factor (VEGF) in corneal neovascularization (CNV), to elucidate the process of CNV formation and, thus, to prepare the ground for further experimental, and clinical studies together with drug treatments.

METHODS

Twelve male Wistar-Albino rats were randomly divided into two groups of six, and two corneas of each rat were used. In all groups, CNV was generated by silver nitrate sticks. At the end of the study, rats were sacrificed by cervical dislocation under ether anaesthesia, and then, their corneas were removed. The expression levels of and in corneas were determined by qRT-PCR array and qRT-PCR. Data analysis was performed using web-based software named PCR array data.

RESULTS

When the corneal samples of rats with CNV were compared to those of the control rats, it was found that a statistically significant difference was present regarding the VEGF level ( < 0.05) with the fold-regulation value> 2. According to the under- and over-expression data in miRNA PCR Array findings of both groups, statistically significant differences were found regarding nine genes with Fold-regulation value <-2 and Fold-regulation value> 2 ( < 0.05). When the corneal samples of the rats with CNV were compared to those of the control rats, statistically significant over-expressions (Fold-regulation value> 2) of and genes were found ( = 0.002443,  = 0.030146,  = 0.000348, respectively). In the same comparison, gene showed statistically significant under-expression with a Fold-regulation value <-2 ( = 0.006428). Also, in the comparison of the two groups, the fold regulation value of the gene was found to be close to - g and statistically significantly under-expressed ( = 0.005082).

CONCLUSION

The over-expressions of and genes, and the under-expression of rno- gene were thought to could play roles in the formation process of CNV by regulation of VEGF-A and through modulation of angiogenesis.