Journal Article

DZNE-2020-03533

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Reactive glia in the injured brain acquire stem cell properties in response to sonic hedgehog. [corrected].

Sirko, S. ; Behrendt, G. ; Johansson, P. A. ; Tripathi, P. ; Costa, M. ; Bek, S. ; Heinrich, C. ; Tiedt, S. ; Colak, D. ; Dichgans, M. ; Fischer, I. R. ; Plesnila, N. ; Staufenbiel, M. ; Haass, C.DZNE* ; Snapyan, M. ; Saghatelyan, A. ; Tsai, L.-H. ; Fischer, A.DZNE* ; Grobe, K. ; Dimou, L. ; Götz, M. (Corresponding author)

2013
Elsevier Amsterdam [u.a.]

This record in other databases:    

Please use a persistent id in citations: doi:10.1016/j.stem.2013.01.019

Abstract: As a result of brain injury, astrocytes become activated and start to proliferate in the vicinity of the injury site. Recently, we had demonstrated that these reactive astrocytes, or glia, can form self-renewing and multipotent neurospheres in vitro. In the present study, we demonstrate that it is only invasive injury, such as stab wounding or cerebral ischemia, and not noninvasive injury conditions, such as chronic amyloidosis or induced neuronal death, that can elicit this increase in plasticity. Furthermore, we find that Sonic hedgehog (SHH) is the signal that acts directly on the astrocytes and is necessary and sufficient to elicit the stem cell response both in vitro and in vivo. These findings provide a molecular basis for how cells with neural stem cell lineage emerge at sites of brain injury and imply that the high levels of SHH known to enter the brain from extraneural sources after invasive injury can trigger this response.

Keyword(s): Animals (MeSH) ; Astrocytes: metabolism (MeSH) ; Astrocytes: pathology (MeSH) ; Brain Injuries: complications (MeSH) ; Brain Injuries: metabolism (MeSH) ; Brain Injuries: pathology (MeSH) ; Cell Death (MeSH) ; Cell Proliferation (MeSH) ; Cell Separation (MeSH) ; Cerebral Cortex: pathology (MeSH) ; Disease Models, Animal (MeSH) ; Gliosis: complications (MeSH) ; Gliosis: pathology (MeSH) ; Hedgehog Proteins: metabolism (MeSH) ; Male (MeSH) ; Mice (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Mutant Strains (MeSH) ; Nerve Tissue Proteins: metabolism (MeSH) ; Neural Stem Cells: metabolism (MeSH) ; Neural Stem Cells: pathology (MeSH) ; Neuroglia: metabolism (MeSH) ; Neuroglia: pathology (MeSH) ; Neurons: metabolism (MeSH) ; Neurons: pathology (MeSH) ; Signal Transduction (MeSH) ; Spheroids, Cellular: metabolism (MeSH) ; Spheroids, Cellular: pathology (MeSH) ; Hedgehog Proteins ; Nerve Tissue Proteins ; neuronal Cdk5 activator (p25-p35)

---

Contributing Institute(s):

1. Molecular Neurodegeneration (AG Haass)
2. Epigenetics and Systems Medicine in Neurodegenerative Diseases (AG Fischer)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2013

---

Database coverage:
; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; IF >= 20 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

---