Role of Rho GTPase in astrocyte morphology and migratory response during in vitro wound healing
Open accessAbstract
Small Rho GTPases are key regulators of the cytoskeleton in a great variety of cells. Rho function mediates morphological changes as well as locomotor activity. Using astrocyte cultures established from neonatal mice we investigated the role of Rho in process formation during astrocyte stellation. Using a scratch‐wound model, we examined the impact of Rho on a variety of morphological and functional variables such as stellation and migratory activity during wound healing. C3 proteins are widely used to study cellular Rho functions. In addition, C3 derived from Clostridium botulinum (C3 bot ) is considered selectively to promote neuronal regeneration. Because the latter requires a balanced activity of neurones and glial cells, the effects of C3 protein on glial cells such as astrocytes have to be considered carefully. Low nanomolar concentrations of C3 proteins significantly promoted process outgrowth and increased process branching. Besides enzymatic inactivation of Rho by ADP‐ribosylation, changes in protein levels of the various Rho GTPases may also contribute to the observed effects. Furthermore, incubation of scratch‐wounded astrocyte cultures with C3 bot accelerated wound healing. By inhibiting the Rho downstream effector ROCK with the selective inhibitor Y27632 we were able to demonstrate that the accelerated wound closure resulted from both enhanced polarized process formation and increased migratory activity of astrocytes into the lesion site. These results suggest that Rho negatively regulates astrocytic process growth and migratory responses after injury and that its inactivation by C3 bot in nanomolar concentrations promotes astrocyte migration.
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In astrocytes, RhoA/ROCK signaling plays a major role in determining astrocyte morphology and reactive state.
“In astrocytes, RhoA/ROCK signaling plays a major role in determining astrocyte morphology and reactive state [118,160,161], and ROCK inhibition reduces reactive gliosis and increases astrocytic expression of prosurvival genes [162,163].”
From RhoA Signaling in Neurodegenerative Diseases (2022) · cites this paper as [161]
The Discussion (page not provided) reports that inhibiting Rho or ROCK changed astrocyte process formation and migration after in vitro injury, supporting a major role in morphology and wound response. Although the paper describes reactive gliosis in its background, it does not establish that RhoA/ROCK determines astrocytes’ overall reactive state. (LLM, conf=0.85)
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Research works printed but not linked: 3
- Aktories K., Barth H. and Just I. (2000) Clostridium botulinum C3 exoenzyme and C3-like transferases, in Handbook of Experimental Pharmacology, Eds: Aktories and Just, pp. 207-233. Springer Verlag, Berlin.
- Ko ¨rnyei Z., Czirok A., Vicsek T. and MadarasZ. E. (2000) Proliferative and migratory responses of astrocytes to in vitro injury. J. Neurosci. Res. 61, 421-429. Astrocyte morphology during wound healing 1247 Ó 2005 International Society for Neurochemistry, J. Neurochem. (2005) 95, 1237-1248 14714159, 2005, 5, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2005.03443.x by Mount Vernon Nazarene University, Wiley Online Library on [17/08/2026]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License · DOI
- Meucci O., Fatatis A., Simen A. A., Bushell T. J., Gray P. W. and Miller R. J. (1998) Chemokines regulate hippocampal neuronal signaling and gp120 neurotoxicity. Proc. Natl Acad. Sci. USA 95, 14 500- 14 505.
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RhoA Signaling in Neurodegenerative Diseases
Schmidt, S. I., Blaabjerg, M., Freude, K., & Meyer, M. (2022) · Cells · doi:10.3390/cells11091520 · Cited by 110 · see citing works
- Authors
- Höltje, M., Hoffmann, A., Hofmann, F., Mucke, C., Große, G., Van Rooijen, N., Kettenmann, H., Just, I., & Ahnert‐Hilger, G.
- Affiliations
- Humboldt-Universität zu Berlin (DE)
- Max Delbrück Center (DE)
- Medizinische Hochschule Hannover (DE)
- Corresponding author
- Höltje, Markus
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2005-09-07
- Volume
- 95
- Issue
- 5
- Pages
- 1237-1248
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2123129865
- Cited by
- 94
- References
- 0
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 3 · 2020: 3 · 2019: 5 · 2018: 1 · 2017: 7 · 2016: 6 · 2015: 6 · 2014: 10 · 2013: 4 · 2012: 4
- FWCI
- 1.75
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- VU Research Portal (publishedVersion)
- Digital Academic REpository of VU University Amsterdam (Vrije Universiteit Amsterdam) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Keywords
- Rho GTPases, astrocytes, astrocyte morphology, astrocyte migration, wound healing, scratch assay, ADP-ribosylation, Rho kinase, Y-27632, cytoskeleton, stellation
- MeSH terms
- Amides, Animals, Animals, Newborn, Astrocytes, Brain, Cell Movement, Cell Survival, Cells, Cultured, Complement C3, Dose-Response Relationship, Drug, Enzyme Inhibitors, Fluorescent Antibody Technique, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Indoles, L-Lactate Dehydrogenase, Liposomes, Pyridines, Recombinant Proteins, Tetrazolium Salts, Time Factors, Wound Healing, rho GTP-Binding Proteins, cdc42 GTP-Binding Protein, Lectins, Cell Size, Cell Proliferation, Mice
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