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Corneal Edema in Inducible Slc4a11 Knockout Is Initiated by Mitochondrial Superoxide Induced Src Kinase Activation.

Diego G Ogando¹, Edward T Kim¹, Shimin Li¹

¹Vision Science Program, School of Optometry, Indiana University, Bloomington, IN 47405, USA.

|June 10, 2023

Summary

This summary is machine-generated.

Inducible Slc4a11 knockout causes corneal edema by impairing corneal endothelium (CE) pump and barrier functions. Oxidative stress and Src kinase activation are key, but treatments like Visomitin and eCF506 show promise in restoring function.

Keywords:

Slc4a11 Src kinase Visomitin barrier function corneal endothelial dystrophy lactate transporters oxidative stress

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Area of Science:

Ophthalmology
Cell Biology
Biochemistry

Background:

The corneal endothelium (CE) is vital for maintaining corneal clarity through its pump and barrier functions.
Slc4a11 plays a critical role in CE function, and its loss leads to corneal edema.
Slc4a11 deficiency causes mitochondrial dysfunction and oxidative stress within the CE.

Purpose of the Study:

To investigate the link between oxidative stress and the failure of CE pump and barrier functions following Slc4a11 knockout.
To evaluate therapeutic approaches for reverting Slc4a11 KO-induced corneal edema.

Main Methods:

Inducible Slc4a11 knockout in mice using Tamoxifen (Tm) administration.
Assessment of corneal thickness, lactate levels, Na+-K+ ATPase activity, and mitochondrial superoxide.
Evaluation of barrier function via fluorescein permeability, ZO-1 integrity, and F-actin morphology.

Main Results:

Slc4a11 knockout rapidly decreased Slc4a11 expression, increased oxidative stress, and induced corneal edema.
CE pump and barrier functions were significantly impaired, with disrupted tight junctions and altered lactate transport.
Activation of Src kinase was observed, correlating with CE dysfunction.
Mitochondrial antioxidant Visomitin and Src kinase inhibitor eCF506 partially restored CE function and reduced edema.

Conclusions:

Slc4a11 knockout-induced oxidative stress activates Src kinase, leading to CE pump and barrier dysfunction.
Targeting oxidative stress and Src kinase activation offers potential therapeutic strategies for corneal edema.