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Inflammation without neuronal death triggers striatal neurogenesis comparable to stroke.

Chapman, Katie LU ; Ge, Ruimin LU ; Monni, Emanuela LU ; Tatarishvili, Jemal LU ; Ahlenius, Henrik LU ; Arvidsson, Andreas LU ; Ekdahl, Christine; Lindvall, Olle LU and Kokaia, Zaal LU (2015) In Neurobiology of Disease 83(Aug 20). p.1-15
Abstract
Ischemic stroke triggers neurogenesis from neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) and migration of newly formed neuroblasts towards the damaged striatum where they differentiate to mature neurons. Whether it is the injury per se or the associated inflammation that gives rise to this endogenous neurogenic response is unknown. Here we showed that inflammation without corresponding neuronal loss caused by intrastriatal lipopolysaccharide (LPS) injection leads to striatal neurogenesis in rats comparable to that after a 30min middle cerebral artery occlusion, as characterized by striatal DCX+ neuroblast recruitment and mature NeuN+/BrdU+ neuron formation. Using global gene expression analysis, changes in several... (More)
Ischemic stroke triggers neurogenesis from neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) and migration of newly formed neuroblasts towards the damaged striatum where they differentiate to mature neurons. Whether it is the injury per se or the associated inflammation that gives rise to this endogenous neurogenic response is unknown. Here we showed that inflammation without corresponding neuronal loss caused by intrastriatal lipopolysaccharide (LPS) injection leads to striatal neurogenesis in rats comparable to that after a 30min middle cerebral artery occlusion, as characterized by striatal DCX+ neuroblast recruitment and mature NeuN+/BrdU+ neuron formation. Using global gene expression analysis, changes in several factors that could potentially regulate striatal neurogenesis were identified in microglia sorted from SVZ and striatum of LPS-injected and stroke-subjected rats. Among the upregulated factors, one chemokine, CXCL13, was found to promote neuroblast migration from neonatal mouse SVZ explants in vitro. However, neuroblast migration to the striatum was not affected in constitutive CXCL13 receptor CXCR5(-/-) mice subjected to stroke. Infarct volume and pro-inflammatory M1 microglia/macrophage density were increased in CXCR5(-/-) mice, suggesting that microglia-derived CXCL13, acting through CXCR5, might be involved in neuroprotection following stroke. Our findings raise the possibility that the inflammation accompanying an ischemic insult is the major inducer of striatal neurogenesis after stroke. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Neurobiology of Disease
volume
83
issue
Aug 20
pages
1 - 15
publisher
Elsevier
external identifiers
  • pmid:26299391
  • wos:000366230000001
  • scopus:84941007478
ISSN
0969-9961
DOI
10.1016/j.nbd.2015.08.013
language
English
LU publication?
yes
id
9b7a7af5-1b2f-456d-81de-0fe684d9f45e (old id 7840191)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/26299391?dopt=Abstract
date added to LUP
2015-09-06 16:49:51
date last changed
2017-10-22 03:23:24
@article{9b7a7af5-1b2f-456d-81de-0fe684d9f45e,
  abstract     = {Ischemic stroke triggers neurogenesis from neural stem/progenitor cells (NSPCs) in the subventricular zone (SVZ) and migration of newly formed neuroblasts towards the damaged striatum where they differentiate to mature neurons. Whether it is the injury per se or the associated inflammation that gives rise to this endogenous neurogenic response is unknown. Here we showed that inflammation without corresponding neuronal loss caused by intrastriatal lipopolysaccharide (LPS) injection leads to striatal neurogenesis in rats comparable to that after a 30min middle cerebral artery occlusion, as characterized by striatal DCX+ neuroblast recruitment and mature NeuN+/BrdU+ neuron formation. Using global gene expression analysis, changes in several factors that could potentially regulate striatal neurogenesis were identified in microglia sorted from SVZ and striatum of LPS-injected and stroke-subjected rats. Among the upregulated factors, one chemokine, CXCL13, was found to promote neuroblast migration from neonatal mouse SVZ explants in vitro. However, neuroblast migration to the striatum was not affected in constitutive CXCL13 receptor CXCR5(-/-) mice subjected to stroke. Infarct volume and pro-inflammatory M1 microglia/macrophage density were increased in CXCR5(-/-) mice, suggesting that microglia-derived CXCL13, acting through CXCR5, might be involved in neuroprotection following stroke. Our findings raise the possibility that the inflammation accompanying an ischemic insult is the major inducer of striatal neurogenesis after stroke.},
  author       = {Chapman, Katie and Ge, Ruimin and Monni, Emanuela and Tatarishvili, Jemal and Ahlenius, Henrik and Arvidsson, Andreas and Ekdahl, Christine and Lindvall, Olle and Kokaia, Zaal},
  issn         = {0969-9961},
  language     = {eng},
  number       = {Aug 20},
  pages        = {1--15},
  publisher    = {Elsevier},
  series       = {Neurobiology of Disease},
  title        = {Inflammation without neuronal death triggers striatal neurogenesis comparable to stroke.},
  url          = {http://dx.doi.org/10.1016/j.nbd.2015.08.013},
  volume       = {83},
  year         = {2015},
}