Wang Fuhua, Sun Xiaolei, Dong Yanling, Cheng Fang, Fan Jiangli, Lu Xiaoqin, Emery Douglas, Shao Hui, Wang Wei, Zhang Lijun, Dean Douglas C, Liu Yongqing
Department of Medicine, University of Louisville, Louisville, Kentucky, United States.
Eye Institute and Eye Hospital of Shangdong First Medical University, Jinan, Shandong Province, China.
Invest Ophthalmol Vis Sci. 2025 Sep 2;66(12):33. doi: 10.1167/iovs.66.12.33.
To characterize Zeb1 regulation of nitrogen mustard (NM)-induced acute corneal epithelial damage and its recovery in mice.
This study utilized topical fluorescein staining and section immunohistochemistry to evaluate NM-induced acute corneal epithelial damage and its recovery in both Zeb1 wild-type and heterozygous knockout mice, as well as real-time quantitative PCR and chromatin immunoprecipitation to delineate the mechanism underlying Zeb1 regulation of such corneal epithelial damage and recovery.
Topical application of NM on the central cornea causes an immediate reduction of Zeb1 expression, followed by de-epithelization and epithelial cell death, along with cell proliferation resulting in epithelial recovery. Monoallelic knockout of Zeb1 decreased NM-induced acute epithelial damage but delayed the recovery from the damage.
Zeb1 facilitates NM-induced corneal epithelial wound healing by maintaining epithelial renewability and thus is a potential therapeutic target to reduce acute mustard gas keratopathy in early ocular pathogenesis.
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