Advanced

Suppression of stroke-induced progenitor proliferation in adult subventricular zone by tumor necrosis factor receptor 1.

Iosif, Robert LU ; Ahlenius, Henrik LU ; Ekdahl, Christine T; Darsalia, Vladimer LU ; Thored, Pär LU ; Jovinge, Stefan LU ; Kokaia, Zaal LU and Lindvall, Olle LU (2008) In Journal of Cerebral Blood Flow and Metabolism 28. p.1574-1587
Abstract
Stroke induced by middle cerebral artery occlusion leads to transiently increased progenitor proliferation in the subventricular zone (SVZ) and long-lasting striatal neurogenesis in adult rodents. Tumor necrosis factor-alpha (TNF-alpha) is upregulated in stroke-damaged brain. Whether TNF-alpha and its receptors influence SVZ progenitor proliferation after stroke is unclear. Here we show that the increased proliferation 1 week after stroke occurred concomitantly with elevated microglia numbers and TNF-alpha and TNF receptor-1 (TNF-R1) gene expression in the SVZ of wild-type mice. TNF receptor-1 was expressed on sorted SVZ progenitor cells from nestin-green fluorescent protein reporter mice. In animals lacking TNF-R1, stroke-induced SVZ cell... (More)
Stroke induced by middle cerebral artery occlusion leads to transiently increased progenitor proliferation in the subventricular zone (SVZ) and long-lasting striatal neurogenesis in adult rodents. Tumor necrosis factor-alpha (TNF-alpha) is upregulated in stroke-damaged brain. Whether TNF-alpha and its receptors influence SVZ progenitor proliferation after stroke is unclear. Here we show that the increased proliferation 1 week after stroke occurred concomitantly with elevated microglia numbers and TNF-alpha and TNF receptor-1 (TNF-R1) gene expression in the SVZ of wild-type mice. TNF receptor-1 was expressed on sorted SVZ progenitor cells from nestin-green fluorescent protein reporter mice. In animals lacking TNF-R1, stroke-induced SVZ cell proliferation and neuroblast formation were enhanced. In contrast, deletion of TNF-R1 did not alter basal or status epilepticus-stimulated cell proliferation in SVZ. Addition of TNF-alpha reduced the size and numbers of SVZ neurospheres through a TNF-R1-dependent mechanism without affecting cell survival. Our results provide the first evidence that TNF-R1 is a negative regulator of stroke-induced SVZ progenitor proliferation. Blockade of TNF-R1 signaling might be a novel strategy to promote the proliferative response in SVZ after stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 21 May 2008; doi:10.1038/jcbfm.2008.47. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Cerebral Blood Flow and Metabolism
volume
28
pages
1574 - 1587
publisher
Nature Publishing Group
external identifiers
  • WOS:000258716400006
  • PMID:18493257
  • Scopus:50249176438
ISSN
1559-7016
DOI
10.1038/jcbfm.2008.47
language
English
LU publication?
yes
id
1ba6ea6e-5290-4c52-9007-fdb73ccdbc8f (old id 1153917)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/18493257?dopt=Abstract
date added to LUP
2008-06-04 10:30:26
date last changed
2016-10-30 04:34:47
@misc{1ba6ea6e-5290-4c52-9007-fdb73ccdbc8f,
  abstract     = {Stroke induced by middle cerebral artery occlusion leads to transiently increased progenitor proliferation in the subventricular zone (SVZ) and long-lasting striatal neurogenesis in adult rodents. Tumor necrosis factor-alpha (TNF-alpha) is upregulated in stroke-damaged brain. Whether TNF-alpha and its receptors influence SVZ progenitor proliferation after stroke is unclear. Here we show that the increased proliferation 1 week after stroke occurred concomitantly with elevated microglia numbers and TNF-alpha and TNF receptor-1 (TNF-R1) gene expression in the SVZ of wild-type mice. TNF receptor-1 was expressed on sorted SVZ progenitor cells from nestin-green fluorescent protein reporter mice. In animals lacking TNF-R1, stroke-induced SVZ cell proliferation and neuroblast formation were enhanced. In contrast, deletion of TNF-R1 did not alter basal or status epilepticus-stimulated cell proliferation in SVZ. Addition of TNF-alpha reduced the size and numbers of SVZ neurospheres through a TNF-R1-dependent mechanism without affecting cell survival. Our results provide the first evidence that TNF-R1 is a negative regulator of stroke-induced SVZ progenitor proliferation. Blockade of TNF-R1 signaling might be a novel strategy to promote the proliferative response in SVZ after stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 21 May 2008; doi:10.1038/jcbfm.2008.47.},
  author       = {Iosif, Robert and Ahlenius, Henrik and Ekdahl, Christine T and Darsalia, Vladimer and Thored, Pär and Jovinge, Stefan and Kokaia, Zaal and Lindvall, Olle},
  issn         = {1559-7016},
  language     = {eng},
  pages        = {1574--1587},
  publisher    = {ARRAY(0xadda9c8)},
  series       = {Journal of Cerebral Blood Flow and Metabolism},
  title        = {Suppression of stroke-induced progenitor proliferation in adult subventricular zone by tumor necrosis factor receptor 1.},
  url          = {http://dx.doi.org/10.1038/jcbfm.2008.47},
  volume       = {28},
  year         = {2008},
}