Absence of Glial Fibrillary Acidic Protein and Vimentin Prevents Hypertrophy of Astrocytic Processes and Improves Post-Traumatic Regeneration
Open accessAbstract
The regenerative capacity of the CNS is extremely limited. The reason for this is unclear, but glial cell involvement has been suspected, and oligodendrocytes have been implicated as inhibitors of neuroregeneration (Chen et al., 2000, GrandPre et al., 2000; Fournier et al., 2001). The role of astrocytes in this process was proposed but remains incompletely understood (Silver and Miller, 2004). Astrocyte activation (reactive gliosis) accompanies neurotrauma, stroke, neurodegenerative diseases, or tumors. Two prominent hallmarks of reactive gliosis are hypertrophy of astrocytic processes and upregulation of intermediate filaments. Using the entorhinal cortex lesion model in mice, we found that reactive astrocytes devoid of the intermediate filament proteins glial fibrillary acidic protein and vimentin (GFAP-/-Vim-/-), and consequently lacking intermediate filaments (Colucci-Guyon et al., 1994; Pekny et al., 1995; Eliasson et al., 1999), showed only a limited hypertrophy of cell processes. Instead, many processes were shorter and not straight, albeit the volume of neuropil reached by a single astrocyte was the same as in wild-type mice. This was accompanied by remarkable synaptic regeneration in the hippocampus. On a molecular level,GFAP-/-Vim-/-reactive astrocytes could not upregulate endothelin B receptors, suggesting that the upregulation is intermediate filament dependent. These findings show a novel role for intermediate filaments in astrocytes and implicate reactive astrocytes as potent inhibitors of neuroregeneration.
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Under baseline conditions, Gfap−/−Vim−/− mice have astrocytes of normal appearance and grossly normal brain anatomy.
“Under baseline conditions, however, Gfap−/−Vim−/− mice have astrocytes of normal appearance and grossly normal brain anatomy (22, 23, 32).”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [23]
Figure 1 and the Results (page not specified in our copy) report similar astrocyte morphology and process length in GFAP−/− Vim−/− and wild-type mice before lesion. The paper does not establish the broader claim that their brain anatomy is grossly normal. (LLM, conf=0.85)
Experimental — accuracy not yet measuredGFAP and Vim are expressed at high levels in activated astrocytes and are critical for the activated phenotype.
“The intermediate filament proteins GFAP and Vim are expressed at high levels in activated astrocytes and are critical for the activated phenotype.”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [23]
The Introduction describes intermediate-filament upregulation as a hallmark of reactive astrocytes and proposes that it is crucial to activation. Figure 1 and the Results show that loss of GFAP and vimentin prevents process hypertrophy and endothelin B receptor upregulation after injury. The paper still calls the deficient astrocytes reactive, so it supports a role in specific features of the activated phenotype, not that these proteins are critical to the activated phenotype as a whole. (LLM, conf=0.84)
Experimental — accuracy not yet measuredWhen Gfap and Vim are both deleted, astrocytes cannot form intermediate filament networks or display reactive morphology.
“But when Gfap and Vim are both deleted, astrocytes cannot form intermediate filament networks or display reactive morphology (22, 23, 32).”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [23]
The Introduction says GFAP/Vim-deficient astrocytes are completely devoid of intermediate filaments. But the Results and Figure 1 describe them as reactive astrocytes with altered morphology and limited process hypertrophy, not as unable to display any reactive morphology. Page numbers are not available in the supplied copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAstrocytes of Gfap−/−Vim−/− mice in the injured area do not develop the characteristic hypertrophy of proximal processes.
“On a cellular level, astrocytes of Gfap−/−Vim−/− mice in the injured area do not develop the characteristic hypertrophy of proximal processes (23).”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [23]
Gfap−/−Vim−/− mice exhibit better posttraumatic regeneration of neuronal synapses and axons, increased baseline and posttraumatic neurogenesis, and improved functional recovery after spinal cord trauma.
“Interestingly, Gfap−/−Vim−/− mice exhibit better posttraumatic regeneration of neuronal synapses (23) and axons (34), increased baseline and posttraumatic neurogenesis (35), and improved functional recovery after spinal cord trauma (36).”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [23]
In several models of acute central nervous system injury, deletion of the genes encoding GFAP and Vim suppresses morphological changes associated with astrocyte activation.
“In several models of acute central nervous system injury, deletion of the genes encoding these proteins suppresses morphological changes associated with astrocyte activation (22, 23, 26, 30, 32, 36).”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [23]
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Molecular dissection of reactive astrogliosis and glial scar formation
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Glia in the pathogenesis of neurodegenerative diseases
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- Authors
- Wilhelmsson, U., Li, L., Pekna, M., Berthold, C.-H., Blom, S., Eliasson, C., Renner, O., Bushong, E., Ellisman, M., Morgan, T. E., & Pekny, M.
- Affiliations
- University of Gothenburg (SE)
- Spanish National Cancer Research Centre (ES)
- University of California San Diego (US)
- University of Southern California (US)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-05-26
- Volume
- 24
- Issue
- 21
- Pages
- 5016-5021
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6729371
- OpenAlex
- W2166851454
- Cited by
- 455
- References
- 126
- Citations by year
- 2026: 14 · 2025: 13 · 2024: 14 · 2023: 12 · 2022: 24 · 2021: 23 · 2020: 31 · 2019: 22 · 2018: 15 · 2017: 18 · 2016: 15 · 2015: 24 · 2014: 26 · 2013: 27 · 2012: 36
- FWCI
- 14.56
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Gothenburg University Publications Electronic Archive (Gothenburg University) (submittedVersion)
- Funders
- Alzheimer's Association
- Swedish Cancer Foundation
- Svenska Sällskapet för Medicinsk Forskning
- Vetenskapsrådet
- National Institutes of Health (RR 04050)
- National Center for Research Resources (RR 04050, P41RR004050, P41 RR04050)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- glial fibrillary acidic protein, vimentin, intermediate filaments, reactive astrocytes, astrocyte hypertrophy, astrocytic processes, nerve regeneration, entorhinal cortex lesion, endothelin B receptor, synaptic regeneration, hippocampus
- MeSH terms
- Animals, Astrocytes, Brain Injuries, Cells, Cultured, Cytoplasm, Glial Fibrillary Acidic Protein, Glutamate-Ammonia Ligase, Hippocampus, Hypertrophy, Mice, Inbred C57BL, Nerve Regeneration, Vimentin, Up-Regulation, Entorhinal Cortex, Receptor, Endothelin B, Mice
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