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T. Miyamoto, S. Saika, K. Fujita, S. Fujita, Y. Ohnishi; Nitric Oxide Synthase 2 Protects Equatorial Lens Cells From Cell Death and Structural Destruction After Ocular Surface Alkali Injury in Mice . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5046.
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© ARVO (1962-2015); The Authors (2016-present)
To evaluate the cytoprotective role of NO synthase 2 in lens injury after ocular surface alkali burn model in mice.
An alkali burn was produced with 1N NaOH in a cornea of Nitric oxide synthase 2 (NOS2) KO/ wild type mice (n=62) under general anesthesia and allowed to heal up to Day 20. The animals were sacrificed and enucleated eye was processed for histology, TUNEL methods to detect an apoptosis or immunohistochemical examination for heat shock protein 70 (HSP70), to detect anti–apoptotic reaction, and phospho–Akt (Ser473) (pAkt) as a survival factor.
Lens epithelial cells were once transformed into fibroblastic cells and then decreased after ocular surface alkali burn both in NOS2 KO mice and wild types. lens cells in equatorial lesion were still remained and kept the structure of lens bow in wild type mice, but a part of cells were dead and the structure of lens bow were destructed in NOS2 KO mice. TUNEL positive cells were more marked in NOS2 KO than in wild type at from 1 to 3 hours after alkali injury. pAkt/HSP70 expression was marked in equatorial lens cells of wild type and less in NOS2 KO mice.
NO synthase 2 may have an important role to protect equatorial lens cells from cell death and to maintain the structure of lens bow after ocular surface alkali injury in mouse lens.
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