Deletion of galectin‐3 exacerbates microglial activation and accelerates disease progression and demise in a SOD1 G93A mouse model of amyotrophic lateral sclerosis
Article Swipe
Bruce J. Lerman
,
Eric P. Hoffman
,
Margaret Sutherland
,
Khaled Bouri
,
Daniel K. Hsu
,
Fu‐Tong Liu
,
Jeffrey D. Rothstein
,
Susan M. Knoblach
·
YOU?
·
· 2012
· Open Access
·
· DOI: https://doi.org/10.1002/brb3.75
YOU?
·
· 2012
· Open Access
·
· DOI: https://doi.org/10.1002/brb3.75
Galectins are pleiotropic carbohydrate‐binding lectins involved in inflammation, growth/differentiation, and tissue remodeling. The functional role of galectins in amyotrophic lateral sclerosis ( ALS ) is unknown. Expression studies revealed increases in galectin‐1 mRNA and protein in spinal cords from SOD1 G93A mice, and in galectin‐3 and ‐9 mRNAs and proteins in spinal cords of both SOD1 G93A mice and sporadic ALS patients. As the increase in galectin‐3 appeared in early presymptomatic stages and increased progressively through to end stage of disease in the mouse, it was selected for additional study, where it was found to be mainly expressed by microglia. Galectin‐3 antagonists are not selective and do not readily cross the blood–brain barrier; therefore, we generated SOD1 G93A / Gal‐3 −/− transgenic mice to evaluate galectin‐3 deletion in a widely used mouse model of ALS . Disease progression, neurological symptoms, survival, and inflammation were assessed to determine the effect of galectin‐3 deletion on the SOD1 G93A disease phenotype. Galectin‐3 deletion did not change disease onset, but resulted in more rapid progression through functionally defined disease stages, more severely impaired neurological symptoms at all stages of disease, and expiration, on average, 25 days earlier than SOD1 G93A / Gal‐3 +/+ cohorts. In addition, microglial staining, as well as TNF ‐α, and oxidative injury were increased in SOD1 G93A / Gal‐3 −/− mice compared with SOD1 G93A / Gal‐3 +/+ cohorts. These data support an important functional role for microglial galectin‐3 in neuroinflammation during chronic neurodegenerative disease. We suggest that elevations in galectin‐3 by microglia as disease progresses may represent a protective, anti‐inflammatory innate immune response to chronic motor neuron degeneration.
Related Topics
Concepts
SOD1
Microglia
Amyotrophic lateral sclerosis
Neuroinflammation
Inflammation
Galectin
Genetically modified mouse
Immunology
Galectin-3
Medicine
Biology
Pathology
Disease
Transgene
Gene
Biochemistry
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1002/brb3.75
- https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/brb3.75
- OA Status
- gold
- Cited By
- 81
- References
- 59
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2028298072
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2028298072Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1002/brb3.75Digital Object Identifier
- Title
-
Deletion of galectin‐3 exacerbates microglial activation and accelerates disease progression and demise in a
SOD1 G93A mouse model of amyotrophic lateral sclerosisWork title - Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2012Year of publication
- Publication date
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2012-07-23Full publication date if available
- Authors
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Bruce J. Lerman, Eric P. Hoffman, Margaret Sutherland, Khaled Bouri, Daniel K. Hsu, Fu‐Tong Liu, Jeffrey D. Rothstein, Susan M. KnoblachList of authors in order
- Landing page
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https://doi.org/10.1002/brb3.75Publisher landing page
- PDF URL
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/brb3.75Direct link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
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goldOpen access status per OpenAlex
- OA URL
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https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/brb3.75Direct OA link when available
- Concepts
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SOD1, Microglia, Amyotrophic lateral sclerosis, Neuroinflammation, Inflammation, Galectin, Genetically modified mouse, Immunology, Galectin-3, Medicine, Biology, Pathology, Disease, Transgene, Gene, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
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81Total citation count in OpenAlex
- Citations by year (recent)
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2025: 5, 2024: 6, 2023: 5, 2022: 9, 2021: 8Per-year citation counts (last 5 years)
- References (count)
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59Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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