Research Projects

Cornea, the first and strongest refracting element in the eye, is crucial for clear vision. A polygonal mosaic of endothelial cells on the posterior surface of the cornea maintains corneal transparency by regulating fluid flow from the anterior chamber into the corneal stroma. An imbalance in hydration control due to corneal endothelial (CE) dysfunction leads to corneal edema and severe vision loss. CE dysfunction can occur due to trauma, surgery, systemic diseases, and endothelial dystrophies. Cells once lost cannot be replaced, making it important to reduce or prevent their loss. Conditions like glaucoma result from an increase in intraocular pressure (IOP), which can be acute or chronic. In the former, the IOP can reach up to 70mmHg, causing severe pain, redness, corneal swelling, and reduced vision. The pressure is brought back to normal using surgical treatment, while the chronic condition can reach up to 30mmHg and not associated with pain or vision loss until much later. Acute pressure increases lead to changes in cell volume, morphology, disruption of the actin cytoskeleton, and tight junction protein ZO-1, rendering the CE layer leakier. The mechanisms through which these cells identify the pressure increase or adapt to the same to maintain corneal function remain unknown. This project aims to determine the role of transient receptor potential (TRP) channels in sensing and regulating CE response to increased IOP. This study will help understand the basic function of CE cells and design treatment strategies to protect and reduce CE loss in patients with high IOP.