Astrocyte reactivity after brain injury—: The role of galectins 1 and 3
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Astrocytes react to brain injury in a heterogeneous manner with only a subset resuming proliferation and acquiring stem cell properties in vitro. In order to identify novel regulators of this subset, we performed genomewide expression analysis of reactive astrocytes isolated 5 days after stab wound injury from the gray matter of adult mouse cerebral cortex. The expression pattern was compared with astrocytes from intact cortex and adult neural stem cells (NSCs) isolated from the subependymal zone (SEZ). These comparisons revealed a set of genes expressed at higher levels in both endogenous NSCs and reactive astrocytes, including two lectins-Galectins 1 and 3. These results and the pattern of Galectin expression in the lesioned brain led us to examine the functional significance of these lectins in brains of mice lacking Galectins 1 and 3. Following stab wound injury, astrocyte reactivity including glial fibrillary acidic protein expression, proliferation and neurosphere-forming capacity were found significantly reduced in mutant animals. This phenotype could be recapitulated in vitro and was fully rescued by addition of Galectin 3, but not of Galectin 1. Thus, Galectins 1 and 3 play key roles in regulating the proliferative and NSC potential of a subset of reactive astrocytes.
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Transcriptomic profiling shows that reactive astrocytes adopt distinct molecular states in different disease models, in different CNS regions, and in brain tumors.
“Such transcriptomic profiling specifically shows that reactive astrocytes adopt distinct molecular states in different disease models48,66–70, in different CNS regions70, and in brain tumors71.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [68]
The Results section, “Injury-Induced Changes of Gene Expression in the Cerebral Cortex GM Astrocytes” (page unavailable), reports transcriptomic differences between reactive and nonreactive astrocytes after cortical injury. The Introduction describes a stab-wound model and comparison with neural stem cells, not reactive astrocytes across different disease models or CNS regions. The brain-tumor clause is attached to citation 71, not this source. (LLM, conf=0.83)
Experimental — accuracy not yet measuredReactive astrocytes are diverse, as demonstrated by transcriptomic profiling of mouse bulk astrocytes or preselected astrocyte populations.
“Likewise, reactive astrocytes are also diverse, as unequivocally demonstrated by microarray-based66–68 and RNAseq-based48,69–71 transcriptomic profiling of mouse bulk astrocytes48,66–70 or of astrocyte populations preselected according to cell-surface markers71.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [68]
The Results section, “Injury-Induced Changes of Gene Expression in the Cerebral Cortex GM Astrocytes” (page unavailable), reports microarray profiling of sorted mouse reactive astrocytes. The Discussion, “Insights from Genomewide Expression Analysis” (page unavailable), describes heterogeneity, but says transcriptomic comparison of the GFAP-positive and GFAP-negative subsets remains to be done. Thus this paper supports the use of transcriptomic profiling and evidence of diversity, but not the claim that profiling itself demonstrated diversity among reactive astrocyte subsets. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTranscriptomic studies suggested complex functional changes in reactive astrocytes, including novel regenerative functions, proliferation, neural stem cell potential, and loss of homeostatic functions.
“These studies also suggested complex functional changes in reactive astrocytes, including novel regenerative functions70, proliferation, and neural stem cell potential68, as well as loss of homeostatic functions66.”
From Reactive astrocyte nomenclature, definitions, and future directions (2021) · cites this paper as [68]
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- Authors
- Sirko, S., Irmler, M., Gascón, S., Bek, S., Schneider, S., Dimou, L., Obermann, J., De Souza Paiva, D., Poirier, F., Beckers, J., Hauck, S. M., Barde, Y., & Götz, M.
- Affiliations
- Helmholtz Munich (DE)
- Ludwig-Maximilians-Universität München (DE)
- Physiological Genomics, Biomedical CenterLudwig‐Maximilians‐University Munich Germany
- Institut Jacques Monod, CNRS‐University Paris DiderotParis France
- Cardiff University (GB)
- Corresponding author
- Götz, Magdalena
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2015-08-06
- Volume
- 63
- Issue
- 12
- Pages
- 2340-2361
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC5042059
- OpenAlex
- W2154592820
- Cited by
- 126
- References
- 100
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 14 · 2023: 12 · 2022: 11 · 2021: 14 · 2020: 7 · 2019: 16 · 2018: 13 · 2017: 16 · 2016: 9
- FWCI
- 5.14
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Glia (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by-nc-nd)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion, cc-by-nc-nd)
- HAL (submittedVersion)
- Site cant be reached (submittedVersion, cc-by-nc-nd)
- Funders
- DFG (SPP 1757 Functional heterogeneity of glia (MG), SFB 871 neural Circuits (MG); HA 6014/2-2 (SMH))
- Synergy Excellence Cluster, the Helmholtz Foundation (ICEMED Alliance) (MG)
- ERC (340793 (MG))
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Galectins and Cancer Biology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- astrocyte activation, brain injury, galectin-1, galectin-3, lectins, astrocyte proliferation, neural stem cells, subventricular zone, stab wounds, cerebral cortex, glial fibrillary acidic protein, neurosphere formation, gene expression profiling
- MeSH terms
- Animals, Astrocytes, Cells, Cultured, Disease Models, Animal, Glial Fibrillary Acidic Protein, Mice, Inbred C57BL, Somatosensory Cortex, Mice, Knockout, Gene Expression Profiling, Galectin 1, Galectin 3, Cell Proliferation, Stem Cell Niche, Neural Stem Cells, Gray Matter
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