The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Spinal cord injury induces endoplasmic reticulum stress with different cell‐type dependent response
Abstract
The mechanisms of injury‐induced apoptosis of neurons within the spinal cord are poorly understood. In this study, we show that spinal cord injury (SCI) induces endoplasmic reticulum stress revealed by the activation of an unbalanced unfolded protein response (UPR). Using a weight‐drop contusion model of SCI, the UPR activation was characterized by a quick transient phosphorylation of alpha subunit of eukaryotic initiation factor 2 soon restored by the up‐regulation of its regulator Gadd 34; an effective cleavage/activation of the ATF6α transcription factor leading to up‐regulation of the canonical UPR target genes Chop, X bp 1 and Grp 78; the presence of the processing of X bp 1 mRNA indicative of inositol requiring kinase 1 activation, and a gradual accumulation of C/EBP homologous transcription factor protein (CHOP) with concomitant caspase‐12 activation. Interestingly, the subcellular distribution of CHOP was found in the nucleus of neurons and oligodendrocytes but in the cytoplasm of astrocytes. Considering the pro‐apoptotic action attributed to this transcription factor, this phenomenon might account for the different susceptibility of cell types to dye after SCI.
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Harding, H. P., Zhang, Y., Bertolotti, A., Zeng, H., & Ron, D. (2000) · Molecular Cell · doi:10.1016/s1097-2765(00)80330-5 · Cited by 2,021
Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys
Crowe, M. J., Bresnahan, J. C., Shuman, S. L., Masters, J. N., & Beattie, M. S. (1997) · Nature Medicine · doi:10.1038/nm0197-73 · Cited by 1,153
Yoshida, H., Okada, T., Haze, K., Yanagi, H., Yura, T., Negishi, M., & Mori, K. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.18.6755-6767.2000 · Cited by 934
Targeted disruption of the chop gene delays endoplasmic reticulum stress-mediated diabetes
Oyadomari, S., Koizumi, A., Takeda, K., Gotoh, T., Akira, S., Araki, E., & Mori, M. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0214550 · Cited by 752
Cited by
Programmed cell death in spinal cord injury pathogenesis and therapy
Shi, Z., Yuan, S., Shi, L., Li, J., Ning, G., Kong, X., & Feng, S. (2021) · Cell Proliferation · doi:10.1111/cpr.12992 · Cited by 293
Involvement of CHOP, an ER-stress apoptotic mediator, in both human sporadic ALS and ALS model mice
Ito, Y., Yamada, M., Tanaka, H., Aida, K., Tsuruma, K., Shimazawa, M., Hozumi, I., Inuzuka, T., Takahashi, H., & Hara, H. (2009) · Neurobiology of Disease · doi:10.1016/j.nbd.2009.08.013 · Cited by 141
Blocking Autophagy in Oligodendrocytes Limits Functional Recovery after Spinal Cord Injury
Saraswat Ohri, S., Bankston, A. N., Mullins, S. A., Liu, Y., Andres, K. R., Beare, J. E., Howard, R. M., Burke, D. A., Riegler, A. S., Smith, A. E., et al. (2018) · The Journal of Neuroscience · doi:10.1523/jneurosci.0679-17.2018 · Cited by 70
Autophagy, and BiP level decrease are early key events in retrograde degeneration of motoneurons
Penas, C., Font-Nieves, M., Forés, J., Petegnief, V, Planas, A., Navarro, X., & Casas, C. (2011) · Cell Death & Differentiation · doi:10.1038/cdd.2011.24 · Cited by 58
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Metadata
- Authors
- Penas, C., Guzmán, M., Verdú, E., Forés, J., Navarro, X., & Casas, C.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2007-05-03
- Volume
- 102
- Issue
- 4
- Pages
- 1242-1255
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2088071603
- Cited by
- 163
- References
- 4
- FWCI
- 1.24
- Type
- journal article
- Language
- en
- Open access
- closed
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- Penas, C., Guzmán, M., Verdú, E., Forés, J., Navarro, X., & Casas, C. (2007). Spinal cord injury induces endoplasmic reticulum stress with different cell‐type dependent response. Journal of Neurochemistry. https://doi.org/10.1111/j.1471-4159.2007.04671.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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