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Knockout of TMEM206 in mice associated with a loss of corneal transparency
Zi-Jian Yang1, Shou-Yue Huang1, Yu-Feng Zhou1
1Department of Ophthalmology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201801, China.
Aim:
To investigate the role of transmembrane protein 206 (TMEM206) in corneal edema in mice by knockout the TMEM206 gene using CRISPR/Cas9 editing technology.
Methods:
TMEM206-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 TMEM206 mice whereas a similar change was not observed in heterozygous TMEM206 mice and wild-type littermates. OCT examination showed that the mean central cornea thickness was 125±5.4 µm in 4 homozygous TMEM206 mice developed corneal edema and 115±1.2 µm in wild-type mice (t=3.468, P<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 (P>0.05). Transmission electron microscopy revealed a disruption in the organization of the collagen fibrils in the central part of the cornea in homozygous TMEM206 mice.
Conclusion:
TMEM206 is associated with corneal edema which caused organizational disruption of collagen fibrils in corneas of mice.
