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Hiroki Ueno, Takaaki Hattori, Yuta Kumagai, Noboru Suzuki, Satoki Ueno; Evaluation of Corneal Stem/Progenitor Cells in leptin deficient mice. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1007.
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© ARVO (1962-2015); The Authors (2016-present)
Diabetic keratopathy (DK) remains difficult to be treated. It can cause corneal persistent epithelial defects, suggesting a role of corneal nerves in maintaining the corneal homeostasis. Leptin deficient mice which are widely accepted as an animal model of mild type-II diabetes mellitus (DM) have sensory nerve conduction deficits, small sensory nerve fiber neuropathy,intra-epidermal sensory nerve fiber loss. The purpose of this study is to investigate whether putative corneal stem/progenitor cells are altered in obese mice and to understand the pathogenesis in obesity and diabetes mice lacking the leptin gene.
12 week-old male mice with mild type II DM (C57 6JHam ob/ob 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. Keratin 19 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 mild type II DM were preferentially thinner and had fewer branches compared to the normal mice. Hes1 and Keratin 19 expression noted with immunostaining was diminished in corneas of diabetes mellitus when compared with normal corneas. Similarly, mRNA expression levels for Hes1 and p75 were decreased in corneas with diabetes.
Our results suggest that corneal stem/progenitor cells could be altered in animal model of obesity and mild 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 mild type II diabetes mellitus and leptin deficient.
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