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Masako Kumada, Masayuki Niwa, Akira Hara, Hiroyuki Matsuno, Hideki Mori, Shigeru Ueshima, Osamu Matsuo, Tetsuya Yamamoto, Osamu Kozawa; Tissue Type Plasminogen Activator Facilitates NMDA-Receptor–Mediated Retinal Apoptosis through an Independent Fibrinolytic Cascade. Invest. Ophthalmol. Vis. Sci. 2005;46(4):1504-1507. doi: 10.1167/iovs.04-0595.
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purpose. To investigate the association between apoptosis and the fibrinolytic system in retinal cell damage.
methods. Tissue type plasminogen activator–deficient (tPA−/−), urokinase type plasminogen activator–deficient (uPA−/−), plasminogen activator inhibitor-1–deficient (PAI-1−/−), α2 antiplasmin–deficient (α2 AP−/−) mice, and their wild-type counterparts were used. Retinal cell damage was induced by intravitreal injection of the excitotoxin N-methyl-d-aspartate (NMDA). The TdT-dUTP terminal nick-end labeling (TUNEL) method was used to examine retinal cell damage.
results. tPA−/− mice were resistant to retinal cell damage caused by administration of NMDA, and PAI-1−/− mice were more injured than their wild-type. No significant difference was observed between uPA−/− or α2 AP−/− and their wild-type mice.
conclusions. The results strongly suggest that endogenous tPA, but not uPA acts as a facilitator in NMDA-induced retinal cell damage, and that its mechanism may not be associated with cleavage of plasminogen into plasmin in the fibrinolytic cascade.
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