| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
Clinically, the diabetic cornea often shows superficial punctate keratopathy and persistent epithelial defect and recurrent epithelial erosion that is considered to be a form of diabetic keratoepithliopathy. We examined immunohistochemically the change of the extracellular matrix in the diabetic cornea. As animal model of a non-insulin-dependent type (type 2) diabetes, Goto-Kakizaki rat were used. Electron microscopic study showed that basement membrane in the diabetic rat often detaches from the basal cell. The number of hemidesmosomes and anchoring fibrils decreased. In the basal cell, the hemidesomosome formation was disturbed in the diabetic cornea. Localization of the main components of basement membrane, laminin, type IV collagen was examined immunohistochemically. In the diabetic cornea the intensity of the immunoreactivity of laminin decreased. But immunoreactivity of type IV collagen did not changed. Other components of basement membrane, fibronectin, HSPG, type VI collagen localized not only in the basement membrane but also in the stroma. No change of these immunoreactivities was observed. In the diabetic cornea the number of long-spacing collagen increased more rapidly than normal cornea in the Descemet's membrane with age. In human, there is a report that type VIII collagen localizes in the long spacing collagen. So we examined the localization of type VIII collagen in the rat cornea. Type VIII collagen localized in Descemet's membrane and increased in the diabetic cornea. These results suggest that decrease of laminin in the basement membrane of corneal epithelium and increase of type VIII collagen in the Descemet's membrane may be one of the causes of the diabetic keratopathy.
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