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Hiroki Ueno, Takaaki Hattori, Yuta Kumagai, Erika Takada, Noboru Suzuki, Satoki Ueno; Evaluation of Corneal Progenitor Cells in Mice with Type II Diabetes Mellitus. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3505.
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© ARVO (1962-2015); The Authors (2016-present)
Diabetic keratopathy (DK) remains difficult to treat. It can cause corneal epithelial defects, suggesting a role of corneal nerves in maintaining the corneal homeostasis. The purpose of this study is to investigate whether putative corneal progenitor cells are altered in type II diabetes mellitus (DM) corneas and to understand the pathogenesis of diabetic keratopathy.
6 week-old male mice with type II DM (C57 BLKS db/db mice) were assessed by beta-III tubulin (neural marker) immunostaining. Real-time polymerase chain reaction was performed to quantify expression of ATP-binding cassette subfamily G member 2 (ABCG2), hairy enhancer of split 1 (Hes1), the low-affinity NGF receptors (p75) as corneal progenitor cell markers. ABCG2 and Hes1 were assessed in type II DM mice and controls by immunofluorescence microscopic studies.
Beta-III tubulin expression detected with immunostaining was decreased in the diabetic corneas. Corneal subbasal plexus of nerve fibers with type II DM were preferentially thinner and had fewer branches compared to the normal mice. Hes1 expression noted with immunostaining was decreased in corneas of diabetes mellitus when compared with normal corneas. Similarly, mRNA expression levels for Hes1, ABCG2 and p75 were decreased in corneas with diabetes. In contrast, the diabetic corneas showed increased mRNA expression levels of Nerve Growth Factor (NGF) compared to those in normal corneas.
Our results suggest that corneal progenitor cells are altered in animal model of type II diabetes mellitus. Our data may provide novel evidence for the close connection between innervation and maintaining corneal progenitor cells and/or the stem cell niche in cases of type II diabetes mellitus.
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