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Cell Tissue Res. 2011 Feb;343(2):399-409. doi: 10.1007/s00441-010-1090-5. Epub 2010 Dec 3.

Regulation of GDF-15, a distant TGFsuperfamily member, in a mouse model of cerebral ischemia.

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1
Institute for Pharmaceutical Biotechnology, University of Applied Science Biberach, Biberach/Riss, Germany.

Abstract

GDF-15 is a novel distant member of the TGFsuperfamily and is widely distributed in the brain and peripheral nervous system. We have previously reported that GDF-15 is a potent neurotrophic factor for lesioned dopaminergic neurons in the substantia nigra, and that GDF-15-deficient mice show progressive postnatal losses of motor and sensory neurons. We have now investigated the regulation of GDF-15 mRNA and immunoreactivity in the murine hippocampal formation and selected cortical areas following an ischemic lesion by occlusion of the middle cerebral artery (MCAO). MCAO prominently upregulates GDF-15 mRNA in the hippocampus and parietal cortex at 3 h and 24 h after lesion. GDF-15 immunoreactivity, which is hardly detectable in the unlesioned brain, is drastically upregulated in neurons identified by double-staining with NeuN. NeuN staining reveals that most, if not all, neurons in the granular layer of the dentate gyrus and pyramidal layers of the cornu ammonis become GDF-15-immunoreactive. Moderate induction of GDF-15 immunoreactivity has been observed in a small number of microglial cells identified by labeling with tomato lectin, whereas astroglial cells remain GDF-15-negative after MCAO. Comparative analysis of the size of the infarcted area after MCAO in GDF-15 wild-type and knockout mice has failed to reveal significant differences. Together, our data substantiate the notion that GDF-15 is prominently upregulated in the lesioned brain and might be involved in orchestrating post-lesional responses other than the trophic support of neurons.

PMID:
21128084
PMCID:
PMC3032194
DOI:
10.1007/s00441-010-1090-5
[Indexed for MEDLINE]
Free PMC Article

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