The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Microglial Cells Contribute to Endogenous Brain Defenses after Acute Neonatal Focal Stroke
Open accessAbstract
Macrophages are viewed as amplifiers of ischemic brain injury, but the origin of injury-producing macrophages is poorly defined. The role of resident brain macrophages—microglial cells—in stroke remains controversial. To determine whether microglial cells exert injurious effects after neonatal focal stroke, we selectively depleted these cells with intracerebral injection of liposome-encapsulated clodronate before transient middle cerebral artery occlusion in postnatal day 7 rats. Phagocytosis of apoptotic neurons by activated microglia was poor in animals with unmanipulated microglia, and depletion of these cells did not increase the number of apoptotic neurons. Lack of microglia increased the brain levels of several cytokines and chemokines already elevated by ischemia–reperfusion, and also increased the severity and volume of injury, suggesting that microglial cells contribute to endogenous protection during the subacute injury phase. Then, to determine whether accumulation of reactive oxygen species in microglia adversely affects phagocytosis of dying neurons and contributes to injury, we delivered reduced glutathione (GSH) into microglia, again using liposomes. Remarkably, pharmacologically increased intracellular GSH concentrations in microglia induced superoxide accumulation in lipid rafts in these cells, further increased the brain levels of macrophage chemoattractants, and exacerbated injury. Together, these data show that microglia are part of the endogenous defense mechanisms and that, while antioxidants can protect the injured neonatal brain, high levels of reducing equivalents in activated microglia, GSH, trigger superoxide production, favor the reorganization of lipids, amplify local inflammation and exacerbate injury.
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Cites
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Selective Ablation of Proliferating Microglial Cells Exacerbates Ischemic Injury in the Brain
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Cited by
Hu, X., Li, P., Guo, Y., Wang, H., Leak, R. K., Chen, S., Gao, Y., & Chen, J. (2012) · Stroke · doi:10.1161/strokeaha.112.659656 · Cited by 1,535
Spangenberg, E., Severson, P. L., Hohsfield, L. A., Crapser, J., Zhang, J., Burton, E. A., Zhang, Y., Spevak, W., Lin, J., Phan, N. Y., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-11674-z · Cited by 939
The role of inflammation in perinatal brain injury
Hagberg, H., Mallard, C., Ferriero, D. M., Vannucci, S. J., Levison, S. W., Vexler, Z. S., & Gressens, P. (2015) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.13 · Cited by 829
Self-citationThe biphasic function of microglia in ischemic stroke
Ma, Y., Wang, J., Wang, Y., & Yang, G.-Y. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2016.01.005 · Cited by 655
Janus-faced microglia: beneficial and detrimental consequences of microglial phagocytosis
Sierra, A., Abiega, O., Shahraz, A., & Neumann, H. (2013) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2013.00006 · Cited by 574
Metadata
- Authors
- Faustino, J. V., Wang, X., Johnson, C. E., Klibanov, A., Derugin, N., Wendland, M. F., & Vexler, Z. S.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-09-07
- Volume
- 31
- Issue
- 36
- Pages
- 12992-13001
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2020577923
- Cited by
- 317
- References
- 43
- FWCI
- 10.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Faustino, J. V., Wang, X., Johnson, C. E., Klibanov, A., Derugin, N., Wendland, M. F., & Vexler, Z. S. (2011). Microglial Cells Contribute to Endogenous Brain Defenses after Acute Neonatal Focal Stroke. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.2102-11.2011
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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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