MicroRNA inhibits corneal neovascularisation
Reviewed by Graham Wallace

MicroRNAs (miR) are small non-coding RNA that target mRNA for destruction. MiR target about 30% of the protein coding genes and fine tune their expression. MiR have been shown to be involved in several cellular processes including cell cycle, tissue development, ageing and immune responses, and implicated as biomarkers in cancer and heart disease. The normal cornea is an avascular tissue, but new vessel growth impairing vision is associated with infection, trauma or chemical challenge. MiR have been linked to angiogenesis in tumours and in the cornea miR-184 and miR-204 have been associated with neovascularisation (NV). MiR184 has been shown to inhibit expression of vascular endothelial growth factor (VEGF) and downstream signalling to inhibit NV. In this paper the authors utilised a mouse model of corneal NV, and biomechanical stress on primary human limbal epithelial cells and microvascular endothelia cells (HMEC). MiR-204 expression was predominantly localised to epithelial cells, and down-regulated in the inflamed cornea and in cells in response to biomechanical stress. Injection of an agomir aimed to mimic the effect of miR-204 inhibited NV and expression of VEGF. Furthermore, overexpression of miR-204 suppressed the proliferation and migration of HMECs. These results suggest that that stress such as suturing could lead to down-regulation of miR-204 and therefore increase the likelihood of corneal NV. Importantly, agomirs and antagomirs of miRs are being tested in several conditions and modulation of miR204 expression may be a future therapeutic approach to inhibit neovascularisation. 

Epithelium-derived miR204 inhibits corneal neovascularisation.
Zhang X, Di G, Dong M, et al.
EXPERIMENTAL EYE RESEARCH
2017;167:122-7.