Abstract
Transient receptor potential (TRP) non-selective cation channels constitute a superfamily, which contains 28 different genes. In mammals, this superfamily is divided into six subfamilies based on differences in amino acid sequence homology between the different gene products. Proteins within a subfamily aggregate to form heteromeric or homomeric tetrameric configurations. These different groupings have very variable permeability ratios for calcium versus sodium ions. TRP expression is widely distributed in neuronal tissues, as well as a host of other tissues, including epithelial and endothelial cells. They are activated by environmental stresses that include tissue injury, changes in temperature, pH and osmolarity, as well as volatile chemicals, cytokines and plant compounds. Their activation induces, via intracellular calcium signalling, a host of responses, including stimulation of cell proliferation, migration, regulatory volume behaviour and the release of a host of cytokines. Their activation is greatly potentiated by phospholipase C (PLC) activation mediated by coupled GTP-binding proteins and tyrosine receptors. In addition to their importance in maintaining tissue homeostasis, some of these responses may involve various underlying diseases. Given the wealth of literature describing the multiple roles of TRP in physiology in a very wide range of different mammalian tissues, this review limits itself to the literature describing the multiple roles of TRP channels in different ocular tissues. Accordingly, their importance to the corneal, trabecular meshwork, lens, ciliary muscle, retinal, microglial and retinal pigment epithelial physiology and pathology is reviewed.
Highlights
The founding member of the transient receptor potential (TRP) protein superfamily was first described in Drosophila
TRPV4 serves as an osmosensor to mediate a regulatory volume decrease (RVD) response to a hypotonic challenge, since knockdown of its expression in human corneal epithelial cells (HCECs) blunts cell volume restoration.[15]
TRPV1 activation contributes to the increases in IL-6 and IL-8 release through nuclear factor kB (NF-kB) activation, since, during exposure to a TRPV1 antagonist, these increases are fully suppressed.[16]. These results suggest that blocking TRPV1 activation during chronic exposure to hypertonic tears in dry eye disease may have therapeutic value in reducing inflammation
Summary
The founding member of the transient receptor potential (TRP) protein superfamily was first described in Drosophila. TRPV3 activation, either by temperatures above 338C or exposure to the selective agonist, carvacrol, induces currents that are, in part, accounted for by increases in Ca2þ influx.[13,14] TRPV4 serves as an osmosensor to mediate a regulatory volume decrease (RVD) response to a hypotonic challenge, since knockdown of its expression in human corneal epithelial cells (HCECs) blunts cell volume restoration.[15] A hallmark of dry eye disease is that the anterior ocular surface is exposed to hypertonic tears.
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