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• W2761508197 abstract "NMDA, a molecule that is capable of producing the loss of retinal ganglia cells (RGCs), has been widely studied; however, the detailed mechanism is not yet clarified. Previously, Wnt/ β -catenin signaling has been suggested to be involved in the NMDA-induced retinopathy. In addition, previous investigations in our group demonstrated the presence of a Wnt/ β -catenin/COX-2 axis in dorsal root ganglions (DRGs). Therefore, here in this paper, we tested whether there is an association of such axis with NMDA-induced RGC loss. Rat retinal damage models generated by intravitreal injection of NMDA were used to measure the expression levels of β -catenin, COX-2, and VEGF in retinas, and the neuron numbers of the retinal GCL of rats were counted. Then, pharmacological tools (MK801, a NMDA receptor inhibitor; Dickkopf homolog 1, a specific inhibitor of the Wnt pathway; NS-398, a COX-2 inhibitor; and bevacizumab, IVB, a VEGF inhibitor) were introduced to evaluate the detailed roles of Wnt/ β -catenin, COX-2, and VEGF in retinopathy of rats. Results demonstrated that all three factors in sequence are positively regulated neuronal loss induced by NMDA. These observations indicated that the Wnt pathway/COX-2/VEGF axis plays a pathogenic role in retinopathy and represented novel therapeutic targets." @default.
• W2761508197 created "2017-10-20" @default.
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• W2761508197 date "2017-01-01" @default.
• W2761508197 modified "2023-10-14" @default.
• W2761508197 title "The Involvement ofβ-Catenin/COX-2/VEGF Axis in NMDA-Caused Retinopathy" @default.
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• W2761508197 doi "https://doi.org/10.1155/2017/9760501" @default.
• W2761508197 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5660823" @default.
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