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Experimental interventions attenuate a conjunctival epidermal metaplasia model.
Yuki Takezawa1, Masayoshi Kamon2, Keiko Hiraki-Kamon2
1Department of Ophthalmology, Graduate School of Medicine, Ehime University, Toon, Japan.
Experimental Eye Research
|April 28, 2024
Summary
Conjunctival metaplasia, a condition causing ocular surface keratinization, can be modeled using iHCjECs. PAX6 reintroduction and treatments like glucocorticoids or serum partially reverse this epidermal change.
Area of Science:
- Ophthalmology
- Cell Biology
- Epithelial Biology
Background:
- The conjunctiva, an ocular epithelium, differs from epidermis primarily through PAX6 expression.
- Conjunctival metaplasia involves keratinization, observed in dry eye and severe ocular surface diseases.
- A novel cell line (iHCjECs) spontaneously undergoes epidermal metaplasia, decreasing PAX6.
Purpose of the Study:
- To investigate conjunctival epidermal metaplasia using an in vitro model (iHCjECs).
- To test the efficacy of PAX6, serum, and glucocorticoid interventions on this metaplasia.
- To explore potential therapeutic strategies for conjunctival keratinization.
Main Methods:
- Established a conditionally immortalized conjunctival epithelial cell line (iHCjECs).
- Induced epidermal metaplasia in iHCjECs, characterized by gene expression changes.
- Administered PAX6, serum, or glucocorticoids to iHCjECs to assess metaplasia reversal.
Main Results:
- iHCjECs spontaneously exhibited epidermal metaplasia with decreased PAX6 expression.
- PAX6 reintroduction upregulated cell adhesion and tight junction genes (e.g., MIR200CHG, CLDN1).
- Glucocorticoids and serum downregulated epidermal genes (e.g., DSG1, SPRR1A/B, KRT1), partially correcting metaplasia.
Conclusions:
- The iHCjEC model effectively replicates conjunctival epidermal metaplasia.
- PAX6, serum, and glucocorticoids show potential for treating conjunctival keratinization.
- Repurposing existing clinical interventions may offer new therapeutic avenues for ocular surface diseases.
