Published in Research

Study finds DED alters how the cornea heals itself post-injury

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2 min read

In a study using mice with dry eye disease (DED), researchers at Washington University School of Medicine in St. Louis have identified proteins that activate the gene SPARC. These proteins are potential new targets for treating and preventing corneal injuries. (via)

Tell me about the SPARC gene.

SPARC promotes the self-renewal of corneal epithelial stem cells and ocular surface restoration. Previous research has shown in a wound healing process in the corneal epithelium and stroma, increased accumulation of SPARC is observed in the regions undergoing repair. (via)

Let's talk about the study.

Researchers conducted single-cell RNA sequencing in mouse models of DED, diabetes, and other conditions. They profiled the mouse corneal epithelium during homeostasis, aging, diabetes, and DED to identify genes vital to maintaining the health of the cornea.

What were the findings?

In mice with DED, the cell types that accomplish homeostatic renewal were conserved but also associated with the activation of cell states that cause “adaptive regeneration.”

SPARC was identified as a marker for adaptive regeneration in DED that induces corneal epithelial wound healing, and higher levels of the SPARC proteins were associated with better healing. (via)

What does this mean?

SPARC, along with other genes, may provide potential therapeutic targets for treating DED and corneal injury.

Anything else?

The study authors noted that if the identified proteins are not able to operate as therapies to activate the corneal epithelium stem cells in DED patients, it may be possible in the future to transplant engineered limbal stem cells to prevent corneal injury in patients with dry eyes.


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