Lacking TRPA1 Cation Channel Impairs Primary Closure of a Stromal Incision Injury in a Mouse Cornea

Area of Science:

• Ophthalmology
• Cell Biology
• Neuroscience

Background:

• The cornea, a sensory tissue, comprises epithelium, keratocytes, endothelium, and extracellular matrix.
• Transient receptor potential ankyrin 1 (TRPA1) is a cation channel activated by stimuli and present in corneal cells.
• TRPA1's role in corneal wound healing following injury is not fully understood.

Purpose of the Study:

• To investigate the role of TRPA1 in corneal stromal wound healing after incision injury in mice.
• To examine the impact of TRPA1 gene knockout on cellular and molecular processes during corneal repair.

Main Methods:

• Corneal incision injury model in wild-type (WT) and TRPA1-knockout (KO) mice.
• Immunohistochemistry for Schwann cell markers (Sox10, Sox2, p75).
• Analysis of TGFβ1 mRNA, p-Smad3, myofibroblast markers, collagen Ia1, and fibronectin expression.
• In vitro fibroblast contractility assay.

Main Results:

• TRPA1 knockout delayed corneal wound closure and the appearance of repair Schwann cells.
• TRPA1 deletion suppressed TGFβ1 signaling, myofibroblast differentiation, and collagen/fibronectin expression.
• Inhibition of TRPA1 reduced TGFβ-induced fibroblast contractility in vitro.

Conclusions:

• TRPA1 plays a significant role in mouse corneal stromal wound healing.
• TRPA1 influences repair Schwann cell generation, TGFβ signaling, and extracellular matrix remodeling.
• Targeting TRPA1 may offer therapeutic potential for corneal injuries.