Damage to the Epithelial Basement Membrane in the Corneas of Diabetic Rabbits

Hatchell, Diane L.; Magolan, Jerome J.; Besson, Michael J.; Goldman, Arnold I.; Pederson, Harlan J.; Schultz, Karen J.

doi:10.1001/archopht.1983.01040010469029

Cited by 55 publications

(34 citation statements)

References 8 publications

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“…In diabetic corneas, only general BM changes have been described. They include BM thickening, decreased stromal penetration of anchoring fibrils, and greater susceptibility of epithelial BM to damage (Hatchell et al 1983;Azar et al 1989). The influence of diabetes on corneal BM/ECM components and integrins was not studied, which prompted us to analyze in detail their distribution patterns in non-DR diabetic and DR corneas.…”

Section: Discussionsupporting

confidence: 43%

“…ulcers, and edema (Hatchell et al 1983;Herse 1988). Other diabetic corneal alterations include increased basement membrane (BM) thickness (Herse 1988;Azar et al 1989), decreased hemidesmosome numbers (Azar et al 1992;Meller et al 1996), impaired endothelial cell function (Saini and Mittal 1996), altered collagen (Sady et al 1995), and abnormal deposition of complement proteins (Weiss et al 1990).…”

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confidence: 42%

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Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy¹

Ljubimov

Huang

et al. 1998

J Histochem Cytochem.

101

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SUMMARYCorneas of diabetic patients have abnormal healing and epithelial adhesion, which may be due to alterations of the corneal extracellular matrix (ECM) and basement membrane (BM). To identify such alterations, various ECM and BM components and integrin receptors were studied by immunofluorescence on sections of normal and diabetic human corneas. Age-matched corneas from 15 normal subjects, 10 diabetics without diabetic retinopathy (DR), and 12 diabetics with DR were used. In DR corneas, the composition of the central epithelial BM was markedly altered, compared to normal or non-DR diabetic corneas. In most cases the staining for entactin/nidogen and for chains of laminin-1 ( ␣1 ␤1 ␥1) and laminin-10 ( ␣5 ␤1 ␥1) was very weak, discontinuous, or absent over large areas. Other BM components displayed less frequent changes. The staining for ␣3 ␤1 (VLA-3) laminin binding integrin was also weak and discontinuous in DR corneal epithelium. Components of stromal ECM remained unchanged even in DR corneas. Therefore, distinct changes were identified in the composition of the epithelial BM in DR corneas. They may be due to increased degradation or decreased synthesis of BM components and related integrins. These alterations may directly contribute to the epithelial adhesion and wound healing abnormalities found in diabetic corneas. (J Histochem Cytochem 46:1033-1041, 1998)

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Section: Discussionsupporting

confidence: 43%

supporting

confidence: 42%

Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy¹

Ljubimov

Huang

et al. 1998

J Histochem Cytochem.

101

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“…Once the cornea is damaged, however, the healing of epithelial wounds is often delayed and epithelial disorders persist. The underlying pathogenesis of diabetic keratopathy is thought to be attributable to an abnormality of the epithelial basement membrane [5,6,9,12].…”

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confidence: 49%

Abnormal light scattering detected by confocal biomicroscopy at the corneal epithelial basement membrane of subjects with Type II diabetes

et al. 2001

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Despite advances in the control of blood sugar concentration in subjects with diabetes mellitus the management of diabetic complications, such as retinopathy, neuropathy, and nephropathy remains a serious clinical problem. A common underlying feature in the pathology of these diabetic complications is an abnormality of the basement membrane, or basal lamina, in the affected tissues [1]. Thus, thickening of the basement membrane in various tissues, including renal glomeruli and tubules, vascular endothelium, perineurium, and bronchial and corneal epithelium has been described in subjects with diabetes mellitus [2±9].The cornea is the outermost surface of the eyeball and has a relatively simple structure comprised of epithelial, stromal, and endothelial layers. The corneal epithelial basement membrane is located beneath the epithelium and does not contain any vascular elements. These anatomic characteristics of the cornea allow the epithelial basement membrane to be examined optically. Diabetologia (2001) AbstractAims/hypothesis. Abnormalities of the basement membrane are thought to contribute to the complications of diabetes. The suitability of the cornea for detecting such abnormalities was assessed by determining its light-scattering index, a quantitative measure of tissue reflectivity in the basement membrane zone, with a confocal biomicroscope.Methods. The light-scattering index was measured in 65 subjects with Type II (non-insulin-dependent) diabetes mellitus and 18 control subjects and was evaluated for its possible relation to the stage of diabetic retinopathy. Diabetic retinopathy was staged by ophthalmoscopic examination as non-diabetic (NDR), simple (SDR), preproliferative (PPDR), or proliferative (PDR).Results. Examination of the cornea layer-by-layer with a confocal biomicroscope did not show any marked differences in morphology between diabetic and control subjects. The LSI (mean SD) was 0.81 0.13, 0.87 0.09, 0.90 0.09, 0.90 0.13, and 1.02 0.25 in control subjects and in diabetic subjects with NDR, SDR, PPDR, or PDR, respectively; the light-scattering index of diabetic subjects with PDR was significantly greater than that of the control subjects (p = 0.001). An LSI greater than 1.0 was detected in 5.6, 6.3, 15.0, 15.4, and 50.0 % of control subjects and of patients with NDR, SDR, PPDR, or PDR, respectively; the percentage of subjects with an LSI greater than 1.0 was significantly increased in diabetic patients with PDR than for control subjects. Conclusion/interpretation. These results suggest that the LSI increases with the stage of diabetic retinopathy, and that measurement of corneal light scattering could provide an index of basement membrane abnormality in people with diabetes. [Diabetologia (2001) 44: 340±345]

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“…Patients with this disease often develop not only diabetic retinopathy but also keratoepitheliopathies, such as superficial punctate keratopathy, recurrent corneal erosion, and persistent epithelial defects. [1][2][3][4] Diabetic keratoepitheliopathy has been attributed to quantitative and qualitative abnormalities in tear secretion, 1 decreased corneal sensitivity, 1,2 and poor adhesion of regenerating epithelial cells. 3 We also found that qualitative abnormalities in tear secretion such as nonuniformity of the tear lipid layer and decreased tear breakup time, and corneal sensitivity were possibly relevant to diabetic keratoepitheliopathy.…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4] Diabetic keratoepitheliopathy has been attributed to quantitative and qualitative abnormalities in tear secretion, 1 decreased corneal sensitivity, 1,2 and poor adhesion of regenerating epithelial cells. 3 We also found that qualitative abnormalities in tear secretion such as nonuniformity of the tear lipid layer and decreased tear breakup time, and corneal sensitivity were possibly relevant to diabetic keratoepitheliopathy. 5 Furthermore, we hypothesized that diabetic patients may show changes in blinking patterns that would affect keratoepitheliopathy.…”

Section: Introductionmentioning

confidence: 99%

Blinking and superficial punctate keratopathy in patients with diabetes mellitus

Inoue

Okugawa

Amano

et al. 2004

Eye

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Aim To evaluate blinking patterns in patients with diabetes mellitus and whether blinking contributes to the formation of superficial punctate keratopathy in diabetic patients. Methods We examined 163 patients with type II diabetes mellitus and 76 without diabetes. Blinks were recorded, analysed using six parameters, and compared between patients with and without diabetes. Multivariate regression analysis was performed to assess the influence of other ocular factors, such as status of tear lipid layer, tear breakup time, corneal sensitivity, the result of cotton thread test, or blinking rate related to superficial punctate keratopathy. Results In patients with diabetes, the average mean and maximum interblinking times were longer, the average coefficient of variation of interblinking time was higher, and the average blinking rates were lower than those in patients without diabetes. Multivariate regression analysis revealed that the status of tear lipid layer and tear breakup time were significantly relevant to superficial punctate keratopathy (Po0.01). Conclusion Interblinking time was longer in diabetic patients, resulting in a decreased blinking rate. The prevalence of superficial punctate keratopathy cannot be predicted from blinking patterns in patients with diabetes.

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Damage to the Epithelial Basement Membrane in the Corneas of Diabetic Rabbits

Cited by 55 publications

References 8 publications

Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy¹

Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy¹

Abnormal light scattering detected by confocal biomicroscopy at the corneal epithelial basement membrane of subjects with Type II diabetes

Blinking and superficial punctate keratopathy in patients with diabetes mellitus

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Damage to the Epithelial Basement Membrane in the Corneas of Diabetic Rabbits

Cited by 55 publications

References 8 publications

Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy1

Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy1

Abnormal light scattering detected by confocal biomicroscopy at the corneal epithelial basement membrane of subjects with Type II diabetes

Blinking and superficial punctate keratopathy in patients with diabetes mellitus

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Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy¹

Human Corneal Epithelial Basement Membrane and Integrin Alterations in Diabetes and Diabetic Retinopathy¹