Knockout of TMEM206 in mice associated with a loss of corneal transparency  

作　　者：Zi-Jian Yang Shou-Yue Huang Yu-Feng Zhou Shun-Chang Sun 

机构地区：[1]Department of Ophthalmology,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 201801,China [2]Department of Laboratory Medicine,Ruijin Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 201801,China

出　　处：《International Journal of Ophthalmology(English edition)》2024年第11期1967-1972,共6页国际眼科杂志（英文版）

基　　金：Supported by National Natural Science Foundation of China(No.31571294).

摘　　要：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±5.4μm in 4 homozygous TMEM206^(-/-)mice developed corneal edema and 115±1.2μm 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.

关 键 词：transmembrane protein 206 KNOCKOUT CORNEA EDEMA MOUSE 

分 类 号：R772.2[医药卫生—眼科]