Investigative ophthalmology & visual science · 2012
Capsaicin-induced corneal sensory denervation and healing impairment are reversed by NGF treatment.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Lambiase Alessandro, Aloe Luigi, Mantelli Flavio, Sacchetti Marta, Perrella Eleonora, Bianchi Patrizia, Rocco Maria Luisa, Bonini Stefano
Аннотация
PURPOSE: We aimed to evaluate the nerve growth factor (NGF) pathway and its influence on corneal healing mechanisms in normal conditions and in an animal model of corneal denervation induced by capsaicin.
METHODS: Peripheral sensory damage was induced in rat pups by subcutaneous injection of capsaicin and the effects evaluated by hot-plate test, corneal nerve count, and tear secretion. Corneal damage was induced in capsaicin-treated and -untreated rats by epithelial scraping. Healing rate; NGF pathway (NGF, tyrosine kinase A [TrkA], p75); and the stem cell marker p63 were evaluated by RT-PCR, ELISA, Western blot, and immunohistochemistry. The effects of exogenous NGF administration as eye drop formulation were also tested.
RESULTS: Capsaicin treatment induced a significant reduction of peripheral sensitivity, corneal innervation, tear secretion, and corneal healing rate. The ocular effects of capsaicin treatment were associated with an NGF pathway alteration. NGF eye drop treatment aided corneal healing mechanisms through a significant increase in the NGF receptors TrkA and p75, and in the stem cell marker p63.
CONCLUSIONS: In this study, we show that an alteration in the NGF pathway is responsible for a delay in corneal healing in an animal model of sensory denervation. Moreover, we show that NGF eye drop administration modulates corneal innervation, epithelial cell healing, and corneal stem cells. These findings may trigger further research on the role of the NGF pathway in limbal stem cell deficiency.
METHODS: Peripheral sensory damage was induced in rat pups by subcutaneous injection of capsaicin and the effects evaluated by hot-plate test, corneal nerve count, and tear secretion. Corneal damage was induced in capsaicin-treated and -untreated rats by epithelial scraping. Healing rate; NGF pathway (NGF, tyrosine kinase A [TrkA], p75); and the stem cell marker p63 were evaluated by RT-PCR, ELISA, Western blot, and immunohistochemistry. The effects of exogenous NGF administration as eye drop formulation were also tested.
RESULTS: Capsaicin treatment induced a significant reduction of peripheral sensitivity, corneal innervation, tear secretion, and corneal healing rate. The ocular effects of capsaicin treatment were associated with an NGF pathway alteration. NGF eye drop treatment aided corneal healing mechanisms through a significant increase in the NGF receptors TrkA and p75, and in the stem cell marker p63.
CONCLUSIONS: In this study, we show that an alteration in the NGF pathway is responsible for a delay in corneal healing in an animal model of sensory denervation. Moreover, we show that NGF eye drop administration modulates corneal innervation, epithelial cell healing, and corneal stem cells. These findings may trigger further research on the role of the NGF pathway in limbal stem cell deficiency.
Предметные рубрики MeSH
AnimalsAnimals, NewbornBlotting, WesternCapsaicinCorneaCorneal InjuriesCranial Nerve DiseasesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayExtracellular Signal-Regulated MAP KinasesEye InjuriesImmunohistochemistryNerve Growth FactorNerve Tissue ProteinsOphthalmic NerveRatsRats, Sprague-DawleyReceptor, trkAReceptors, Growth FactorReceptors, Nerve Growth FactorReverse Transcriptase Polymerase Chain ReactionSensory System AgentsSympathectomy, ChemicalWound HealingWounds, Nonpenetrating