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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/7840191
- author
- 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
- organization
- publishing date
- 2015
- 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
- pmid:26299391
- 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
- 2016-04-01 10:48:55
- date last changed
- 2022-04-20 06:25:18
@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}},
doi = {{10.1016/j.nbd.2015.08.013}},
volume = {{83}},
year = {{2015}},
}