AI Article Synopsis
- Retinal ganglion cells (RGCs) are crucial for vision and their death contributes to various eye diseases, but the exact mechanisms behind their death are not well understood.
- In this study, researchers used a lab model to induce cell death in RGCs derived from human stem cells through a process called hypoxia-reoxygenation, finding that RGC death was primarily due to apoptosis (programmed cell death).
- This new model allows for testing the effectiveness of apoptosis inhibitors and neuroprotective agents, which could lead to advancements in treating eye diseases in the future.
Article Abstract
Retinal ganglion cells (RGCs) are specialized projection neurons that constitute part of the retina, and the death of RGCs causes various eye diseases, but the mechanism of RGC death is still unclear. Here, we induced cell death in human induced pluripotent stem cell (hiPSC)-derived RGC-rich retinal tissues using hypoxia-reoxygenation in vitro. Flow cytometry, immunochemistry, and Western blotting showed the apoptosis and necrosis of RGCs under hypoxia-reoxygenation, and they were rescued by an apoptosis inhibitor but not by a necrosis inhibitor. This revealed that the cell death induced in our model was mainly due to apoptosis. To our knowledge, this is the first model to reproduce ischemia-reperfusion in hiPSC-derived RGCs. Thus, the efficacy of apoptosis inhibitors and neuroprotective agents can be evaluated using this model, bringing us closer to clinical applications.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10814087 | PMC |
| http://dx.doi.org/10.3390/cells13020130 | DOI Listing |
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