Investigative ophthalmology & visual science · 2025
Zeb1 Facilitates Nitrogen Mustard-Induced Corneal Epithelial Wound Healing by Maintaining Epithelial Renewability.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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История · было → стало
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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
Аннотация
PURPOSE: To characterize Zeb1 regulation of nitrogen mustard (NM)-induced acute corneal epithelial damage and its recovery in mice.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
Предметные рубрики MeSH
AnimalsMechlorethamineEpithelium, CornealWound HealingMiceZinc Finger E-box-Binding Homeobox 1Mice, KnockoutDisease Models, AnimalReal-Time Polymerase Chain ReactionEye BurnsCell ProliferationMice, Inbred C57BLChemical Warfare AgentsHomeodomain ProteinsBurns, ChemicalGene Expression RegulationImmunohistochemistry