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Related Experiment Video

Updated: May 8, 2026

Effect of Artificial Tear Formulations on the Metabolic Activity of Human Corneal Epithelial Cells after Exposure to Desiccation

Effect of Artificial Tear Formulations on the Metabolic Activity of Human Corneal Epithelial Cells after Exposure to Desiccation

Published on: May 2, 2020

Tryptase compromises corneal epithelial barrier function.

Qiyan Li¹, Ying Jie, Cong Wang

¹Beijing Ophthalmol and Vis Sci Key Lab, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.

Cell Biochemistry and Function

|September 3, 2013

Summary

This summary is machine-generated.

Tryptase compromises corneal epithelial barrier function by increasing matrix metalloproteinase-9 (MMP9) expression. This disrupts cellular processes and damages the corneal barrier, a finding relevant to corneal health research.

Keywords:

cornea epithelial barrier function epithelial cells matrix metalloprotease tryptase

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Area of Science:

Ophthalmology
Cell Biology
Biochemistry

Background:

Corneal epithelial barrier dysfunction negatively impacts ocular health.
The precise mechanisms underlying this dysfunction remain largely unknown.
Understanding these mechanisms is crucial for developing effective treatments.

Purpose of the Study:

To investigate the role of tryptase in compromising corneal epithelial barrier function.
To elucidate the specific molecular pathways involved in tryptase-induced barrier damage.
To identify potential therapeutic targets for restoring corneal barrier integrity.

Main Methods:

Utilized a human corneal epithelial cell line (HCE cells) cultured as monolayers.
Quantified matrix metalloproteinase-9 (MMP9) expression using qRT-PCR and Western blotting.
Assessed endosome/lysosome fusion via confocal microscopy and barrier function using a Transwell system.

Main Results:

Human corneal epithelial cells express proteinase-activated receptor-2 (PAR2).
Tryptase activation of PAR2 upregulated MMP9 expression in HCE cells.
Tryptase interfered with endosome/lysosome fusion and compromised epithelial barrier function.
Pretreatment with an MMP9 inhibitor prevented tryptase-induced barrier dysfunction.

Conclusions:

Tryptase significantly increases MMP9 expression in corneal epithelial cells.
This MMP9 upregulation leads to impaired endosome/lysosome fusion and compromised barrier function.
Targeting MMP9 may offer a therapeutic strategy for corneal epithelial barrier defects.