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Endogenous TSG-6 Modulates Corneal Inflammation Following Chemical Injury

Overview
Journal Ocul Surf
Specialty Ophthalmology
Date 2023 Dec 27
PMID 38151073
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Abstract

Purpose: Tumor necrosis factor (TNF)-stimulated gene-6 (TSG-6) is upregulated in various pathophysiological contexts, where it has a diverse repertoire of immunoregulatory functions. Herein, we investigated the expression and function of TSG-6 during corneal homeostasis and after injury.

Methods: Human corneas, eyeballs from BALB/c (TSG-6), TSG-6 and TSG-6 mice, human immortalized corneal epithelial cells and murine corneal epithelial progenitor cells were prepared for immunostaining and real time PCR analysis of endogenous expression of TSG-6. Mice were subjected to unilateral corneal debridement or alkali burn (AB) injuries and wound healing assessed over time using fluorescein stain, in vivo confocal microscopy and histology.

Results: TSG-6 is endogenously expressed in the human and mouse cornea and established corneal epithelial cell lines and is upregulated after injury. A loss of TSG-6 has no structural and functional effect in the cornea during homeostasis. No differences were noted in the rate of corneal epithelial wound closure between BALB/c, TSG-6 and TSG-6 mice. TSG-6 mice presented decreased inflammatory response within the first 24 h of injury and accelerated corneal wound healing following AB when compared to control mice.

Conclusion: TSG-6 is endogenously expressed in the cornea and upregulated after injury where it propagates the inflammatory response following chemical injury.

Citing Articles

Progranulin Facilitates Corneal Repair Through Dual Mechanisms of Inflammation Suppression and Regeneration Promotion.

Yan D, Zhang Y, Huang Y, Ouyang W Inflammation. 2024; 47(5):1648-1666.

PMID: 38460093 DOI: 10.1007/s10753-024-01999-3.

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