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Eduardo M Rocha, Lara Dias, Jayter Silva Paula, Larissa Ferreira, Jacqueline Faustino, Ana Carolina Dias; Transient receptor potential vanilloid type 1 (TRPV1) related-responses to ocular surface agression. Invest. Ophthalmol. Vis. Sci. 2016;57(12):393.
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© ARVO (1962-2015); The Authors (2016-present)
Corneal diseases are leading causes of blindness. Repair mechanisms are largely concentrated in the epithelium, but targets for therapeutic interventions are poorly understood. In aggressions to the corneal epithelium, the activation of transient receptors of potential vanilloid 1 (TRPV1) leads to inflammatory and wound healing signaling. This study identifies the TRPV1-related inflammatory and histological responses in the cornea of rats and mice.
Real time PCR investigation was applied on cornea and lacrimal gland (LG) after nocioceptive or inflammatory stimuli to identify cytokines and TRPV-1 in animal models of diabetes mellitus (DM) benzalkonium chloride 0.2% (BAC) toxicity. Mice TRPV1-/- compared to control C57 naive or under single stimulation with 1 µM Capsaicin (CAP), BAC 0.2% for 7 days or after the alkali burn (NaOH 1 M). Histology evaluated LG, cornea and trigeminal ganglion (TG) on those groups.
In rats with DM the expression of IL-1β and IL-6 mRNA was reduced in the cornea (p=0.0159, for both DM and BAC), and TNF-α on BAC group (p=0.0159). The TRPV1-/- mice have normal ocular and physical phenotype, but lower sensitivity to CAP 1μM (p=0.0095). BAC decreased tear secretion compared to controls (p=0.0079). TRPV1-/- mice group presented better corneal healing with no evidence of cornea or TG histological changes after injury.
DM and BAC recognized as neuropathic effectors, decrease the expression of inflammatory mediators but not TRPV1. TRPV1-/- does not change the phenotype or cytokines after moderate aggression (BAC), but result in lower pain sensation and improved wound healing of the cornea.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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