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Glia. 2015 Dec;63(12):2340-61. doi: 10.1002/glia.22898. Epub 2015 Aug 6.

Astrocyte reactivity after brain injury-: The role of galectins 1 and 3.

Author information

1
Physiological Genomics, Biomedical Center, Ludwig-Maximilians-University Munich, Germany.
2
Institute of Stem Cell Research, Helmholtz Center Munich, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
3
Institute of Experimental Genetics, Helmholtz Center Munich, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
4
Research Unit Protein Science, Helmholtz Center Munich, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
5
Department of Physiology, Federal University of Sao Paulo, Sao Paulo, Brazil.
6
Institut Jacques Monod, CNRS-University Paris Diderot, Paris, France.
7
Chair of Experimental Genetics, Center of Life and Food Sciences Weihenstephan, Technische Universität München, Freising-Weihenstephan, Germany.
8
School of Biosciences, Cardiff University, Cardiff, United Kingdom.
9
SYNERGY, Excellence Cluster of Systems Neurology, Ludwig-Maximilians-University Munich, Germany.

Abstract

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.

KEYWORDS:

genomewide analysis; glia proliferation; neurosphere

PMID:
26250529
PMCID:
PMC5042059
DOI:
10.1002/glia.22898
[Indexed for MEDLINE]
Free PMC Article

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