Essential protective roles of reactive astrocytes in traumatic brain injury.

By D. Myer, G. Gurkoff, S. M. Lee, David A. Hovda, M. Sofroniew. Brain : a journal of neurology, 2006

630 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/430024b9a61e87fe99b0018356f3f93aa61134d4

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. M. Sofroniew
2. M. Pekny
3. M. Pekna
4. David J. Loane
5. J. Burda
6. M. Schwartz
7. H. Vinters
8. Federico E. Turkheimer

In Neurology

1. M. Sofroniew
2. M. Pekny
3. J. Burda
4. M. Pekna
5. E. Hol
6. Alok Kumar
7. Alexei Verkhratsky
8. Y. Ao

Citations in the corpus

• The bright side of the glial scar in CNS repair (2009, background): “, as well as the neuronal degeneration that follows traumatic brain injur”
• Astrocytes: Key Regulators of Neuroinflammation. (2016, background): “" [12]”
• Astrocytes: biology and pathology (2009, background): “As reviewed in detail elsewhere [226], many studies using transgenic and experimental animal models provide compelling evidence that reactive astrocytes protect CNS cells and tissue by (1) uptake of potentially excitotoxic glutamate [33, 198, 234], (2) protection from oxidative stress via glutathion”
• Inflammation after trauma: Microglial activation and traumatic brain injury (2011, background): “This could be due to the astrocytic response to TBI enclosing and isolating the damaged area.(27) Alternatively, microglia may persist at the site of focal lesions but downregulate expression of TSPO over time.”
• Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, positive): “…performance exacerbates neuronal dysfunction following brain injury and transgenic ablation of reactive astrocytes increases neuronal cell death and promotes worse outcome after TBI (Myer et al., 2006); this may in part reflect the loss of ability to limit the influx of inflammatory cells.”
• Astrocyte roles in traumatic brain injury (2015, background): “Such focal lesions can vary considerably in size, and can encompass large areas or can be restricted to small clusters of cells (Myer et al., 2006; Villapol et al., 2014).”
• Astrocytes: a central element in neurological diseases (2016, background): “For example, transgenic ablation or prevention of astrogliosis or astrocyte scar formation causes increased inflammation and tissue damage and worsens functional outcome in all CNS insult models studies thus far, including traumatic injury, ischemic injury (stroke), infection, autoimmune inflammatio”
• Glial Scar Borders Are Formed by Newly Proliferated, Elongated Astrocytes That Interact to Corral Inflammatory and Fibrotic Cells via STAT3-Dependent Mechanisms after Spinal Cord Injury (2013, background): “…of treatment with ganciclovir exhibit no detectable detrimental effects of transgene expression such that brain structure and histology, including the appearance of astrocytes, are indistinguishable from nontransgenic littermates (Bush et al., 1998, 1999; Faulkner et al., 2004; Myer et al., 2006).”
• STAT3 is a critical regulator of astrogliosis and scar formation after spinal cord injury (2008, background): “…scar formation is to prevent the migration of activated inflammatory cells away from the lesion site into closely adjacent potentially viable neural tissue, based on transgenically targeted astrocyte ablation studies (Bush et al., 1999; Faulkner et al., 2004; Sofroniew, 2005; Myer et al., 2006).”