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S. Sugaya, T. Sakimoto, M. Sawa; p75NTR (Neurotrophin Receptor) and RECK (Reversion Inducing Cysteine-Rich Protein With Kazal Motifs) Expression in Keratoconus Cornea. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3530.
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To investigate p75NTR (neurotrophin receptor) and RECK (reversion inducing cysteine-rich protein with Kazal motifs) expression in keratoconus cornea.
Four keratoconus cornea and 4 non-keratoconus cornea (3 corneal leukoma and 1 macular corneal dystrophy) were investigated. Corneal buttons were obtained at the time of penetrating keratoplasty and immunohistochemistry was performed with antibodies against p75NTR. RNA was extracted and RT (reverse transcriptional)-PCR was performed for RECK gene expression.
p75NTR expression was detected at basal layer of corneal epithelium in keratoconus cornea. The non-keratoconus cornea showed weak p75 immunoreactivity compared with keratoconus cornea. In RT-PCR, RECK expression was detected in non-keratoconus cornea but absent in keratoconus cornea.
RECK is the metalloproteinase inhibitor that has been attracted attention for its down-regulation in cancer-adjacent tissue and is reported to be a specific inhibitor of ADAM (a disintegrin and metalloproteinase)10. p75NTR is nerve growth factor receptor and is regulated by ADAM17-induced ectodomain shedding. In previous report, p75NTR expression is reported to be absent in corneal epithelium and RECK expression is not yet reported in the cornea. Through the present results of p75NTR up-regulation and RECK down-regulation in keratoconus cornea, it may be considered that ADAM-mediated proteins relate to pathophysiology of keratoconus.
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