Knockout of in mice associated with a loss of corneal transparency.

AIM

To investigate the role of transmembrane protein 206 (TMEM206) in corneal edema in mice by knockout the gene using CRISPR/Cas9 editing technology.

METHODS

-knockout mice were generated using the CRISPR-Cas9 system. Variations in ophthalmic pathology were observed using slit lamp microscope and optical coherence tomography (OCT), intraocular pressure (IOP) was measured using a TonoLab Rebound Tonometer, and the ultrastructure of the corneal was observed using a transmission electron microscope.

RESULTS

Corneal opacity was observed in 4/18 homozygous mice whereas a similar change was not observed in heterozygous mice and wild-type littermates. OCT examination showed that the mean central cornea thickness was 125±5.4 µm in 4 homozygous mice developed corneal edema and 115±1.2 µm in wild-type mice (=3.468, <0.05) at 43wk. The mean IOP was 12.08±0.07 mm Hg in four right eyes with corneal edema and 12.03±0.03 mm Hg in three normal left eyes (>0.05). Transmission electron microscopy revealed a disruption in the organization of the collagen fibrils in the central part of the cornea in homozygous mice.

CONCLUSION

TMEM206 is associated with corneal edema which caused organizational disruption of collagen fibrils in corneas of mice.