OMIX

Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis

OMIX401

1Summary
Title Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis
Description Forkhead box C1 (FOXC1) is required for neural crest and ocular development, and mutations in FOXC1 lead to inherited Axenfeld-Rieger syndrome. Here, we find that FOXC1 and paired box 6 (PAX6) are co-expressed in the human limbus and central corneal epithelium. Deficiency of FOXC1 and alternation in epithelial features occur in patients with corneal ulcers. FOXC1 governs the fate of the corneal epithelium by directly binding to lineage-specific open promoters or enhancers marked by H3K4me2. FOXC1 depletion not only activates the keratinization pathway and reprograms corneal epithelial cells into skin-like epithelial cells but also disrupts the collagen metabolic process and interferon signaling pathways. Loss of interferon regulatory factor 1 (IRF1) and PAX6 induced by FOXC1 dysfunction is linked to the corneal ulcer. Collectively, our results reveal a FOXC1-mediated regulatory network responsible for corneal epithelial homeostasis and provide a potential therapeutic target for corneal ulcer.
Organism Homo sapiens
Data Type -
Data Accessibility Open-access
BioProject PRJCA005255
Release Date 2021-06-25
Submitter Hong Ouyang (Ouyhong3@mail.sysu.edu.cn)
Organization Zhongshan Ophthalmic Center, Sun Yat-sen University
Submission Date 2021-06-25
2Files & Download

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File ID File Title Number/Samples File Type File Size File Suffix Download Times Download
OMIX401-20-01 dCEC_scramble and shFOXC1_TPM values 3 Transcriptomic 3.2 MB rar 37
OMIX401-64-02 FOXC1 Epigenomics bed 6 Epigenome-Wide Association Study (EWAS) 4.6 MB rar 70

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