Abstract
Optimal vision requires an ocular surface with vital epithelial coverage and a stable tear film. A multitude of endogenous and external factors may alter this delicate balance. Studies over the last decade have established that Ca2+ is an important factor in the control of ocular surface epithelial function and has led to the identification of critical components. In particular, transient receptor potential channels (TRPs) have been identified as important components in corneal and conjunctival cells. These channels encompass a group of ion channels of numerous cell types. TRPs are nonselective cation channels which are Ca2+ permeable. Most TRPs serve as thermosensitive molecular sensors (thermo-TRPs). Our Ca2+ imaging and patch-clamp studies indicate that the activity of two TRP isoforms, TRPV1 and TRPM8, can be modulated by changes in external temperature osmolarity and some endogenous substrates. These TRPs are expressed on both non-neuronal and neuronal corneal cells. Furthermore, these interactions affect control of cytokines either promoting or inhibiting inflammation, one of the key findings in dry eye syndrome. Taken together, these results not only lead to a better understanding of the pathophysiology in pain and inflammation reactions on the surface of the eye, but these studies may also offer new avenues to understand the pathophysiology of the disease and support the development of novel therapeutic targets in dry eye syndrome.
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