Cornea · 2006
EMMPRIN and MMP-1 in keratoconus.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Seppälä Hannu P S, Määttä Marko, Rautia Mikko, Mackiewicz Zygmunt, Tuisku Ilpo, Tervo Timo, Konttinen Yrjö T
Аннотация
PURPOSE: This study was conducted to determine the eventual presence and activity of EMMPRIN (extracellular matrix metalloproteinase inducer CD147) and interstitial collagenase MMP-1 in the cornea of keratoconus patients and their eventual interrelationship. MMP-1 was chosen because it is able to degrade fibrillar corneal collagens type I and III and might therefore play a role in stromal thinning in keratoconus.
METHODS: Immunohistochemical labeling of EMMPRIN and MMP-1 in relation to histopathological changes in 5 keratoconus patients and 5 matched healthy controls was investigated.
RESULTS: Relatively strong EMMPRIN expression was found in normal corneal epithelial cells, but moderate expression was also found in stroma. In keratoconus, EMMPRIN was found in all layers of cornea, especially in histopathologically altered areas. In normal cornea, MMP-1 staining was weak and restricted to epithelial cells. In keratoconus, MMP-1 expression was slightly augmented in epithelial cells and also appeared locally in a scattered manner in the stroma. The distribution of MMP-1 did not totally overlap with that of histologically apparent corneal damage and EMMPRIN expression.
CONCLUSIONS: Both EMMPRIN and MMP-1 are upregulated in keratoconus, but MMP-1 may not be the only tissue destructive MMP upregulated by EMMPRIN as only EMMPRIN expression correlated topologically very well with corneal damage.
METHODS: Immunohistochemical labeling of EMMPRIN and MMP-1 in relation to histopathological changes in 5 keratoconus patients and 5 matched healthy controls was investigated.
RESULTS: Relatively strong EMMPRIN expression was found in normal corneal epithelial cells, but moderate expression was also found in stroma. In keratoconus, EMMPRIN was found in all layers of cornea, especially in histopathologically altered areas. In normal cornea, MMP-1 staining was weak and restricted to epithelial cells. In keratoconus, MMP-1 expression was slightly augmented in epithelial cells and also appeared locally in a scattered manner in the stroma. The distribution of MMP-1 did not totally overlap with that of histologically apparent corneal damage and EMMPRIN expression.
CONCLUSIONS: Both EMMPRIN and MMP-1 are upregulated in keratoconus, but MMP-1 may not be the only tissue destructive MMP upregulated by EMMPRIN as only EMMPRIN expression correlated topologically very well with corneal damage.