Role of surface ectoderm-specific mitofusin 2 in the corneal morphologic development of mice

Mitofusin 2 ( ) mediates the mitochondrial fusion in dynamic balance between mitochondrial fission and fusion. This study aimed to investigate the role of in mice corneal dysplasia with conditional knockout (CKO) technique. The CKO mice model was established with the system. Each offspring of ; ( CKO) mice and Mfn2 ( WT) mice was identified by polymerase chain reaction (PCR). Macroscopic observation, immunohistostaining and HE staining were used to evaluate the corneal morphologic development in CKO mice and WT mice. The cells proliferation and apoptosis were detected by BrdU labeling and TUNEL assay. Real-time PCR was used to detect mRNA expression of corneal markers (K12, Col1α1, Pax6, keratocan and NSE). Results showed that CKO mice showed increased corneal thickness, small eyeball from E15.5 to P60 and small eye crack after birth. The corneal stromal thickness significantly increased in CKO mice, and the random arrangement fibers of the corneal stroma increased in CKO mice. The proliferative cells in the cornea of CKO mice were less than in WT mice while the apoptotic cells in the cornea of CKO mice were increased. K12 and Pax6 expression decreased in the cornea and the Col1α1 expression increased in CKO mice as compared to WT mice. The expression of corneal stromal marker Col1α1 in the CKO mice was significantly higher than that in the WT mice. Corneal thickness was mainly caused by corneal stroma collagen proliferation. In conclusion, deletion affects corneal development, especially because of collagen hyperplasia in the corneal stroma.