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Y. Okada, S. Saika, K. Shirai, M. Miyajima, W. W. Kao, P. Reinach; Reduced Inflammation and Scarring During Corneal Wound Healing in TRPV1 Knockout Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2939.
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© ARVO (1962-2015); The Authors (2016-present)
The transient receptor potential vanilloid subtype 1 (TRPV1) is functionally expressed in human corneal epithelial cells (HCEC). It is activated by noxious stimuli (including acidity, endocanabinoids, lipoxygenase products, heat) and capsaicin, a component of red pepper extracts. Since TRPV1 activation induces proinflammatory cytokine release in HCEC, we determined in TRPV1 knockout mice if corneal wound healing following alkali burn-injury was associated with reduced inflammation and scarring.
Three microliters of 1 N NaOH were applied to the right eye of 6-8 week TRPV1 (-/-) (KO) or TRPV1 (+/+)(WT) mice to produce an ocular surface alkali burn under general anesthesia. Eyes of 28 KO and 28 WT mice were subsequently histologically examined at 1, 2. 5. 10, 20 days. Immunohistochemistry was conducted by using an antibody against either alpha-SMA, F4/80 macrophage antigen or myeloperoxidase (MPO) for neutrophil recruitment.
From 1 to 20 days after an alkali burn, corneal stromas of the KO mice were more transparent and thinner as compared with those of WT mice. HE histological examination indicated more marked inflammation and stromal thickening in the WT mice corneas than in the KOs. Immunohistochemical staining of alpha-SMA, F4/80 and MPO was markedly less in the KO corneas during the aforementioned period.
Absence of TRPV1 expression and function in mice reduces inflammation and scarring during the corneal wound healing process following an alkalai burn.
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