| First Author | Kumada M | Year | 2004 |
| Journal | Toxicol Appl Pharmacol | Volume | 200 |
| Issue | 1 | Pages | 48-53 |
| PubMed ID | 15451307 | Mgi Jnum | J:93533 |
| Mgi Id | MGI:3057243 | Doi | 10.1016/j.taap.2004.03.017 |
| Citation | Kumada M, et al. (2004) Endogenous tissue type plasminogen activator facilitates NMDA-induced retinal damage. Toxicol Appl Pharmacol 200(1):48-53 |
| abstractText | To investigate the role of tissue plasminogen activator (tPA) in retinal damage, tPA-deficient and wild-type mice were employed. Two different retinal neuron insult models were used in the present study. One is an excitotoxin-treated retinal model, created by direct intravitreal injection of glutamate analogs, NMDA or kainic acid (KA), and the other is an ischemia-reperfusion model induced by transient elevation of intraocular pressure. TdT-dUTP terminal nick-end labeling (TUNEL) method was used to examine the retinal cell nuclear damage. The number of TUNEL-positive cells in ganglion cell layer (GCL) and inner nuclear layer (INL) in tPA-deficient mice after low-, but not high-dose NMDA was significantly less compared to wild type. In contrast, neither intravitreal KA or transient ischemia produced significant difference in retinal damage in tPA vs. wild-type mice. These data show that tPA-deficient mice are resistant to retinal damage by intravitreal injection of NMDA, and indicate that tPA plays a role in the retinal cell damage induced by excitotoxins, especially NMDA. |
