The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Increased Production of Tumor Necrosis Factor-α by Glial Cells Exposed to Simulated Ischemia or Elevated Hydrostatic Pressure Induces Apoptosis in Cocultured Retinal Ganglion Cells
Open accessAbstract
Although glial cells in the optic nerve head undergo a reactivation process in glaucoma, the role of glial cells during glaucomatous neurodegeneration of retinal ganglion cells is unknown. Using a coculture system in which retinal ganglion cells and glial cells are grown on different layers but share the same culture medium, we studied the influences of glial cells on survival of retinal ganglion cells after exposure to different stress conditions typified by simulated ischemia and elevated hydrostatic pressure. After the exposure to these stressors, we observed that glial cells secreted tumor necrosis factor-α (TNF-α) as well as other noxious agents such as nitric oxide into the coculture media and facilitated the apoptotic death of retinal ganglion cells as assessed by morphology, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and caspase activity. The glial origin of these noxious effects was confirmed by passive transfer experiments. Furthermore, retinal ganglion cell apoptosis was attenuated ∼66% by a neutralizing antibody against TNF-α and 50% by a selective inhibitor of inducible nitric oxide synthase (1400W). Because elevated intraocular pressure and ischemia are two prominent stress factors identified in the eyes of patients with glaucoma, these findings reveal a novel glia-initiated pathogenic mechanism for retinal ganglion cell death in glaucoma. In addition, these findings suggest that the inhibition of TNF-α that is released by reactivated glial cells may provide a novel therapeutic target for neuroprotection in the treatment of glaucomatous optic neuropathy.
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Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.
Gavrieli, Y., Sherman, Y., & Ben-Sasson, S. A. (1992) · The Journal of cell biology · doi:10.1083/jcb.119.3.493 · Cited by 9,444
Handbook of fluorescent probes and research chemicals
Haugland, R. P. (1996) · Medical Entomology and Zoology · Cited by 2,793
NITRIC OXIDE: A Physiologic Messenger Molecule
Bredt, D. S., & Snyder, S. H. (1994) · Annual Review of Biochemistry · doi:10.1146/annurev.bi.63.070194.001135 · Cited by 2,368
Brewer, G. J., Torricelli, J. R., Evege, E. K., & Price, P. J. (1993) · Journal of Neuroscience Research · doi:10.1002/jnr.490350513 · Cited by 2,325
The TNF receptor 1-associated protein TRADD signals cell death and NF-κB activation
Hsu, H., Xiong, J., & Goeddel, D. V. (1995) · Cell · doi:10.1016/0092-8674(95)90070-5 · Cited by 2,012
Reactive astrocytes: cellular and molecular cues to biological function
Ridet, J. L., Privat, A., Malhotra, S. K., & Gage, F. H. (1997) · Trends in Neurosciences · doi:10.1016/s0166-2236(97)01139-9 · Cited by 1,766
Activation of microglial cells by β-amyloid protein and interferon-γ
Meda, L., Cassatella, M. A., Szendrei, G. I., Otvos, L., Baron, P., Villalba, M., Ferrari, D., & Rossi, F. (1995) · Nature · doi:10.1038/374647a0 · Cited by 1,314
Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis.
Quigley, H. A., Nickells, R. W., Kerrigan, L. A., Pease, M. E., Thibault, D., & Zack, D. J. (1995) · PubMed · Cited by 935
Cytokines and the nervous system II: actions and mechanisms of action
Rothwell, N. J., & Hopkins, S. J. (1995) · Trends in Neurosciences · doi:10.1016/0166-2236(95)93890-a · Cited by 923
Tumor Necrosis Factor-α: A Mediator of Focal Ischemic Brain Injury
Barone, F. C., Arvin, B., White, R. F., Miller, A., Webb, C. L., Willette, R. N., Lysko, P. G., & Feuerstein, G. Z. (1997) · Stroke · doi:10.1161/01.str.28.6.1233 · Cited by 863
Cited by
Bringmann, A., Iandiev, I., Pannicke, T., Wurm, A., Hollborn, M., Wiedemann, P., Osborne, N. N., & Reichenbach, A. (2009) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2009.07.001 · Cited by 761
Inflammation in Glaucoma: From the back to the front of the eye, and beyond
Baudouin, C., Kolko, M., Melik-Parsadaniantz, S., & Messmer, E. M. (2021) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2020.100916 · Cited by 454
Role of Nitric Oxide in Inflammation‐Mediated Neurodegeneration
LIU, B., GAO, H., WANG, J., JEOHN, G., COOPER, C. L., & HONG, J. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb04077.x · Cited by 425
Inherited glaucoma in DBA/2J mice: Pertinent disease features for studying the neurodegeneration
LIBBY, R. T., ANDERSON, M. G., PANG, I.-H., ROBINSON, Z. H., SAVINOVA, O. V., COSMA, I. M., SNOW, A., WILSON, L. A., SMITH, R. S., CLARK, A. F., et al. (2005) · Visual Neuroscience · doi:10.1017/s0952523805225130 · Cited by 409
Wang, M., Ma, W., Zhao, L., Fariss, R. N., & Wong, W. T. (2011) · Journal of Neuroinflammation · doi:10.1186/1742-2094-8-173 · Cited by 228
Metadata
- Authors
- Tezel, G., & Wax, M. B.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2000-12-01
- Volume
- 20
- Issue
- 23
- Pages
- 8693-8700
- ISSN
- 0270-6474
- 1529-2401
- OpenAlex
- W1624269173
- Cited by
- 395
- References
- 63
- FWCI
- 14.05
- Type
- journal article
- Language
- en
- Open access
- green
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- Tezel, G., & Wax, M. B. (2000). Increased Production of Tumor Necrosis Factor-α by Glial Cells Exposed to Simulated Ischemia or Elevated Hydrostatic Pressure Induces Apoptosis in Cocultured Retinal Ganglion Cells. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.20-23-08693.2000
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