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:
https://lup.lub.lu.se/record/1153917
- author
- 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
- organization
- publishing date
- 2008
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neurology, Lund (013027000), Hematopoietic Stem Cell Laboratory (013022012), Faculty of Medicine (000022000)
- 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
- 2016-04-04 09:17:13
- date last changed
- 2022-07-24 21:46:17
@article{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 = {{Nature Publishing Group}},
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}},
doi = {{10.1038/jcbfm.2008.47}},
volume = {{28}},
year = {{2008}},
}