Change in Long-Spacing Collagen in  
                        Descemet's Membrane of Diabetic Goto-Kakizaki Rats  
                        and Its Suppression by Antidiabetic Agents

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Abstract

We examined changes in the ultrastructure and localization of major extracellular matrix components, including 5 types of collagen (type I, III, IV, VI, and VIII), laminin, fibronectin, and heparan sulfate proteoglycan in Descemet's membrane of the cornea of diabetic GK rats. In the cornea of diabetic GK rats, more long-spacing collagen fibrils were observed in Descemet's membrane than in the membrane of the nondiabetic Wistar rats. Both GK and Wistar rats showed an age-dependent increase in the density of the long-spacing collagen. Immunoelectron microscopy showed that type VIII collagen was localized in the internodal region of the long-spacing collagen, which was not labelled by any of the other antibodies used. The antidiabetic agents nateglinide and glibenclamide significantly suppressed the formation of the long-spacing collagen in the diabetic rats. Long-spacing collagen would thus be a useful indicator for studying diabetic changes in the cornea and the effect of antidiabetic agents.

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Most cited references 54

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Ultrastructure of the trabecular meshwork in untreated cases of primary open-angle glaucoma (POAG).

Allison M. Meyer, I Grierson, E Drecoll … (1993)

Thirty-one trabeculectomy specimens of patients suffering from primary open-angle glaucoma (POAG) who had received no, or only minor, medication prior to surgery were ultrastructurally and quantitatively analysed. Most of the specimens revealed thickened trabeculae, increased amounts of plaque-material deposited within the cribriform layer and an abundance of long spacing (lattice) collagen. The uveal meshwork was partly deprived of cells whereas the cribriform layer often contained numerous enlarged, light cells with many small mitochondria and lysosomes but no prominent endoplasmic reticulum or Golgi complexes. The quantitation of sheath-deprived plaque material (SD plaques) in a defined area of inner and outer wall of Schlemm's canal showed no significant difference between the untreated cases studied here and the treated ones studied previously. However, both groups had significantly higher amounts of SD plaque material in the inner wall than normal controls of a similar age range.

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Corneal endothelial changes in type I and type II diabetes mellitus.

Richard O. Schultz, Mamoru Matsuda, Richard W. Yee … (1984)

Forty-six corneas from 25 patients who had had type II (adult-onset) diabetes for more than ten years were examined by specular microscopy with quantitative morphometric analyses of individual endothelial cells. Thirty-four corneas from 21 age-matched nondiabetic subjects were examined for comparison. We also examined 31 corneas from 17 patients with type I (juvenile-onset) diabetes and compared them to 41 corneas from 23 age-matched normal volunteers. The corneal endothelium in type II diabetes showed no difference in cell density but demonstrated a significantly higher coefficient of variation, a decrease in the percentage of hexagonal cells, and a low figure coefficient compared to an age-matched nondiabetic population. Type I diabetes produced similar cell changes, but these changes occurred in the earlier decades. Moreover, we detected a significantly higher rate of cell loss in type I diabetes, resulting in a significant decrease in cell density in the fourth and fifth decades. These results clearly indicate that the diabetic endothelium is morphologically abnormal. The observed anatomic changes result in a less stable and more vulnerable cell layer, possibly explaining some of the persistent clinical changes in the diabetic cornea after surgical trauma.

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Fuchs corneal dystrophy: aberrant collagen distribution in an L450W mutant of the COL8A2 gene.

W. H. Bell, Ö Sundin, M W Stark … (2005)

To characterize histologically Descemet's membrane in an early-onset Fuchs corneal dystrophy (FCD) COL8A2 mutant and compare these findings with corneas from late-onset FCD and normal corneas. A corneal explant from a patient with the L450W COL8A2 mutation and others with late-onset disease were studied with antibodies to collagens IV, VIIIA1, VIIIA2, fibronectin, and laminin. Transmission electron microscopy was performed on a portion of the explant. Control explants included eye bank corneas without known disease and surgical explants from unrelated conditions. In normal corneas, a regular array of colocalized COL8A1 and COL8A2 was observed in the anterior half of Descemet's membrane. In the L450W mutant, Descemet's membrane was several times thicker than normal and traversed by refractile strands and blebs that stained intensely for COL8A2, a feature also observed in late-onset FCD. Both the alpha1 and alpha2 subtypes of collagen VIII were observed at high levels along the anterior edge of Descemet's, another abnormal feature also found in late-onset FCD. Ultrastructure of the L450W cornea revealed a well-formed anterior banded layer more than three times thicker than normal. An unusual, thin internal layer was rich in patches of wide-spaced collagen. The layer is a distinctive pathologic structure that is associated with FCD and is characterized by approximately 120 nm periodicity and the presence of collagen VIII. Depositions of collagen IV, fibronectin, and laminin were also greatly increased in the of posterior Descemet's membrane, yet another general feature shared between early- and late-onset disease. Early-onset COL8A2 L450W disease involves massive accumulation and abnormal assembly of collagen VIII within Descemet's membrane, a process that is presumed to begin during fetal development. Both early- and late-onset subtypes of FCD appear to be the result of abnormal basement membrane assembly rather than a primary defect in endothelial metabolism.

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Author and article information

Journal

Journal ID (nlm-ta): Exp Diabetes Res

Journal ID (publisher-id): EDR

Title: Experimental Diabetes Research

Publisher: Hindawi Publishing Corporation

ISSN (Print): 1687-5214

ISSN (Electronic): 1687-5303

Publication date (Print): 2008

Publication date (Electronic): 2 September 2008

Volume: 2008

Electronic Location Identifier: 818341

Affiliations

¹Department of Anatomy, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan

²Department of Anatomy, Yokohama City University School of Medicine, Kanazawa Ku, Fukuura 3-9, Yokohama, Kanagawa 236-0004, Japan

³Department of Biochemistry, Kyorin University School of Medicine, Mitaka, Tokyo 181-8611, Japan

Author notes

*Yoshihiro Akimoto: yakimoto@ 123456kyorin-u.ac.jp

Recommended by Timothy Kern

Article

DOI: 10.1155/2008/818341

PMC ID: 2528061

PubMed ID: 18779868

SO-VID: 0ee2e64a-4804-496c-8fe9-ffa5b33bc9ad

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.