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(Investigative Ophthalmology and Visual Science. 2005;46:1504-1507.)
© 2005 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.04-0595
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Tissue Type Plasminogen Activator Facilitates NMDA-Receptor–Mediated Retinal Apoptosis through an Independent Fibrinolytic Cascade

Masako Kumada,1,2 Masayuki Niwa,1,3 Akira Hara,4 Hiroyuki Matsuno,1 Hideki Mori,4 Shigeru Ueshima,5 Osamu Matsuo,5 Tetsuya Yamamoto,2 and Osamu Kozawa1

1From the Departments of Pharmacology, 2Ophthalmology, and 4Tumor Pathology, and the 3Medical Education Development Center, Gifu Graduate University School of Medicine, Gifu, Japan; and the 5Department of Physiology, Kinki University School of Medicine, Osaka-Sayama, Japan.

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–/–), {alpha}2 antiplasmin–deficient ({alpha}2 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 {alpha}2 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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