Redefining the concept of reactive astrocytes as cells that remain within their unique domains upon reaction to injury
By U. Wilhelmsson, E. Bushong, D. Price, Benjamin L Smarr, Van Phung, M. Terada, Mark Ellisman, M. Pekny. Proceedings of the National Academy of Sciences of the United States of America, 2006
616 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Neurology
View Paper: https://www.semanticscholar.org/paper/1614034d00a275be48dc7fd9e9022d403153c891
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Citations in the corpus
- The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “Generally, astrocytosis has most commonly been marked by varying upregulation of the intermediate filament decorating proteins glial fibrillary acidic protein (GFAP) and vimentin (422), hypertrophy of the primary branches (373, 412), expansion of normally defined astrocytic domains at the site of in”
- NOX4 promotes ferroptosis of astrocytes by oxidative stress-induced lipid peroxidation via the impairment of mitochondrial metabolism in Alzheimer's diseases (2021, background): “Regarding the form of astrocytes, reactive astrocytes are an activated form of astrocytes in response to toxic materials [49].”
- Astrocytes: biology and pathology (2009, background): “In mild or moderate reactive astrogliosis there is variable up regulation of expression of GFAP and other genes [226], as well as hypertrophy of cell body and processes that can vary in degree but that occurs within the domains of individual astrocytes [257] without substantive inter-”
- Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “While astrocytes around the CNS lesion in GFAP / Vim / mice are comparable to those of wild-type mice with respect to their number and the volume they access (262), they do not develop the typical reactivephenotypecharacterizedby the thickening (hypertrophy) of their main cellular processes (260, 26”
- Toll-like receptor 4 is required for α-synuclein dependent activation of microglia and astroglia (2013, background): “Furthermore, astroglia react to various CNS insults, such as infection, injury, and neurodegeneration, with morphological changes and variations in the molecular expression pattern (Wilhelmsson et al., 2006).”
- Genomic Analysis of Reactive Astrogliosis (2012, background): “Reactive astrocytes undergo dramatic morphological changes (Wilhelmsson et al., 2006), and various alterations in gene expression have been observed (Sofroniew, 2009).”
- 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): “…regards changes in cell morphology, proliferation, and molecular expression, which are tuned in a context-specific manner to different CNS insults (Hatten et al., 1991; Norton et al., 1992; Wilhelmsson et al., 2006; Oberheim et al., 2008; Sofroniew, 2009; Hamby et al., 2012; Zamanian et al., 2012).”
- Astrocyte reactivity: Subtypes, states and functions in CNS innate immunity (2020, background): “Notably, the discrete, non-overlapping cellular domains exhibited by astrocytes in healthy grey matter are preserved such that hypertrophy occurs primarily within these individual cellular domains [51].”
- Astrocytes: a central element in neurological diseases (2016, background): “Astrocytes around the CNS lesion in GFAP−/−Vim−/− mice are present in normal numbers and form normally tiled domains [252], but do not develop the typical hypertrophy of the main cellular processes [250, 252].”
- Origin and progeny of reactive gliosis: A source of multipotent cells in the injured brain (2008, background): “Astrocytes react to brain injury by hypertrophy of their somata and processes (5), increased synthesis of glial-fibrillary acidic protein (GFAP), or reexpression of the progenitor markers vimentin and nestin (2, 6).”