February 1999
Volume 40, Issue 2
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Articles  |   February 1999
A possible role for p16INK4 in neuronal cell death after retinal ischemia-reperfusion injury.
Author Affiliations
  • S Kuroiwa
    Department of Ophthalmology, Shinshu University School of Medicine, Matsumoto, Japan.
  • N Katai
    Department of Ophthalmology, Shinshu University School of Medicine, Matsumoto, Japan.
  • N Yoshimura
    Department of Ophthalmology, Shinshu University School of Medicine, Matsumoto, Japan.
Investigative Ophthalmology & Visual Science February 1999, Vol.40, 528-533. doi:
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    • Get Citation

      S Kuroiwa, N Katai, N Yoshimura; A possible role for p16INK4 in neuronal cell death after retinal ischemia-reperfusion injury.. Invest. Ophthalmol. Vis. Sci. 1999;40(2):528-533.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To study whether cell type-specific death occurs in retinal ischemia-reperfusion injury and the possible roles of p16INK4 in the determination of cell death. METHODS: Retinal ischemia-reperfusion injury was induced in rats by a ligation method. After 1 hour of ischemia and a time of reperfusion that varied, rat eyes were enucleated. Cell death in the retina was studied by the TdT-dUTP terminal nick-end labeling method and propidium iodide (PI) staining. Electron microscopic observation of the retina was also performed. Immunohistochemical studies using antibodies against syntaxin and calbindin were performed to detect amacrine cells and horizontal cells, respectively, and immunohistochemical studies using an antibody against p16INK4 were performed to study whether this cell cycle-related protein was expressed in dying cells. RESULTS: Most of the calbindin-positive horizontal cells in the outer aspect of the inner nuclear layer (INL) showed morphologic features of necrosis. In contrast, syntaxin-positive amacrine cells in the inner aspect of the INL showed features of apoptosis. Of 320 calbindin-positive horizontal cells, only 11 (3.4%) showed positive PI staining. Those calbindin-positive, horizontal cells were p16INK4 positive. In contrast, 746 of 910 (82.0%) syntaxin-positive amacrine cells showed condensed PI staining, and none were p16INK4 positive. CONCLUSIONS: Expression of p16INK4 may regulate the fate of retinal neurons in ischemia-reperfusion injury, and cell type-specific death thus occurs in the retina after such injury.

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