Conditional ablation of Stat3 or Socs3 discloses a dual role for reactive astrocytes after spinal cord injury
By Seiji Okada, M. Nakamura, H. Katoh, Tamaki Miyao, T. Shimazaki, K. Ishii, J. Yamane, A. Yoshimura, Y. Iwamoto, Y. Toyama and 1 more. Nature Medicine, 2006
934 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Genetics
View Paper: https://www.semanticscholar.org/paper/381a5e5272b30ba9c6292557b35ed94d5e6d81f3
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Citations in the corpus
- Astrocytes: a central element in neurological diseases (2016, positive): “resulted in a better functional recovery [158].”
- Spinal Cord Injury Reveals Multilineage Differentiation of Ependymal Cells (2008, background): “]. Modulating the responsiveness to axonal growth-inhibitory factors and glial scar formation are attractive strategies to improve functional recovery after central nervous system injuries [”
- Reactive gliosis and the multicellular response to CNS damage and disease (2014, positive): “or decrease lesion sizes (Brambilla et al., 2005; Herrmann et al., 2008; Okada et al., 2006; Wanner et al., 2013), providing targets for potential intervention.”
- Origin and progeny of reactive gliosis: A source of multipotent cells in the injured brain (2008, background): “R gliosis as the response of the CNS to injury is instrumental for sealing off the injured tissue, promoting tissue integrity and restricting inflammation and neuronal death (1, 2).”
- Origin of new glial cells in intact and injured adult spinal cord. (2010, background): “However, astrocytes shield the intact tissue from further damage and limit the infiltration of inflammatory cells and further demyelination (Faulkner et al., 2004; Okada et al., 2006).”
- From basics to clinical: a comprehensive review on spinal cord injury. (2014, background): “These sequence of events consequently lead to worst functional outcomes (Faulkner et al., 2004; Okada et al., 2006).”
- Neuroinflammation and depression: A review (2020, background): “Similar to microglial cells, astrocytes express common pattern recognition receptors (PRRs) to combat CNS threats and are able to switch to an activated state (Guttenplan & Liddelow, 2019), for example, through lipopolysaccharide (LPS) challenge (Okada et al., 2006).”
- Astrocytes: Key Regulators of Neuroinflammation. (2016, background): “Together these findings indicate that STAT3 signaling in astrocytes regulates those aspects of astrogliosis essential for restricting inflammation and lesion size [61] (Figures 1 and 2).”
- STAT3 is a critical regulator of astrogliosis and scar formation after spinal cord injury (2008, background): “…2000; Albrecht et al., 2002; Nakamura et al., 2003), (2) tissue levels of pSTAT3 levels increase after SCI (Yamauchi et al., 2006), and (3) broad deletion of STAT3 from neural cells using a nestin-Cre transgenic model increases lesion size and attenuates recovery after SCI (Okada et al., 2006).”
- Self-Assembling Nanofibers Inhibit Glial Scar Formation and Promote Axon Elongation after Spinal Cord Injury (2008, background): “…axonal regeneration after SCI, astrogliosis after CNS injury also serves beneficial functions, such as repairing the blood– brain barrier and reducing infiltration by circulating cells (Bush et al., 1999; Faulkner et al., 2004; Okada et al., 2006), which may be critical for restoring homeostasis.”
- The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “The STAT signaling pathway has also been implicated in astrocytosis to initiate hypertrophy (FIGURE 5A) (165, 291, 408).”
- Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “In contrast, following spinal cord lesions, mice with nestin promoter-driven ablation of Socs3, a negative feedback molecule of STAT3 (74, 151), showed increased phosphorylation of STAT3, increased astrocyte migration, more prominent contraction of the lesion area, and better functional recovery com”