Selective depletion of Mac-1-expressing microglia in rat subventricular zone does not alter neurogenic response early after stroke.
Heldmann, Ursula LU ; Mine, Yutaka LU ; Kokaia, Zaal LU
; Ekdahl Clementson, Christine
LU
and Lindvall, Olle
LU
(2011)
In Experimental Neurology
229.
p.391-398
- Abstract
- Ischemic stroke induces migration of newly formed neuroblasts, generated by neural stem cells in the adult rat subventricular zone (SVZ), towards the injured striatum where they differentiate into mature neurons. Stroke also leads to accumulation of microglia in the SVZ but their role for neurogenesis is unclear. Here we developed a method for selective depletion of the macrophage antigen complex-1 (Mac-1)-expressing microglia population in the SVZ by intraventricular injection of the immunotoxin Mac-1-saporin in rats. We found that the vast majority of Mac-1+ cells were Iba-1+ microglia. The Mac-1+ population was heterogeneous and included both a small proliferative pool of cells, which was not affected by middle cerebral artery occlusion... (More)
- Ischemic stroke induces migration of newly formed neuroblasts, generated by neural stem cells in the adult rat subventricular zone (SVZ), towards the injured striatum where they differentiate into mature neurons. Stroke also leads to accumulation of microglia in the SVZ but their role for neurogenesis is unclear. Here we developed a method for selective depletion of the macrophage antigen complex-1 (Mac-1)-expressing microglia population in the SVZ by intraventricular injection of the immunotoxin Mac-1-saporin in rats. We found that the vast majority of Mac-1+ cells were Iba-1+ microglia. The Mac-1+ population was heterogeneous and included both a small proliferative pool of cells, which was not affected by middle cerebral artery occlusion (MCAO), and a larger subpopulation that changed morphologically into a semi-activated state in response to the insult. This subpopulation did not increase its expression of the phagocytic marker ED1 but exhibited high levels of triggering receptor expressed on myeloid cells-2 (TREM-2), associated with alternative microglia activation. A minor portion of the SVZ Mac-1+ cells originated from the blood early after stroke, but this macrophage population became much more substantial at later stages. Almost 80% reduction of Mac-1-expressing microglia, caused by Mac-1 saporin delivered just before and at 1week after MCAO, did not alter the numbers of newly formed neuroblasts in the striatum or their migratory distance. These findings indicate that the Mac-1-expressing microglia in the SVZ do not play a major role either for the number of neuroblasts which exit the SVZ or their migration in the striatum early following stroke. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1883740
- author
- Heldmann, Ursula
LU
; Mine, Yutaka
LU
; Kokaia, Zaal
LU
; Ekdahl Clementson, Christine
LU
and Lindvall, Olle
LU
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Experimental Neurology
- volume
- 229
- pages
- 391 - 398
- publisher
- Academic Press
- external identifiers
-
- wos:000291419400024
- pmid:21419118
- scopus:79956152659
- ISSN
- 0014-4886
- DOI
- 10.1016/j.expneurol.2011.03.005
- language
- English
- LU publication?
- yes
- id
- ac58c3a7-66b9-4597-86f6-4d053815233b (old id 1883740)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/21419118?dopt=Abstract
- date added to LUP
- 2016-04-01 09:51:52
- date last changed
- 2025-02-04 02:53:30
@article{ac58c3a7-66b9-4597-86f6-4d053815233b,
abstract = {{Ischemic stroke induces migration of newly formed neuroblasts, generated by neural stem cells in the adult rat subventricular zone (SVZ), towards the injured striatum where they differentiate into mature neurons. Stroke also leads to accumulation of microglia in the SVZ but their role for neurogenesis is unclear. Here we developed a method for selective depletion of the macrophage antigen complex-1 (Mac-1)-expressing microglia population in the SVZ by intraventricular injection of the immunotoxin Mac-1-saporin in rats. We found that the vast majority of Mac-1+ cells were Iba-1+ microglia. The Mac-1+ population was heterogeneous and included both a small proliferative pool of cells, which was not affected by middle cerebral artery occlusion (MCAO), and a larger subpopulation that changed morphologically into a semi-activated state in response to the insult. This subpopulation did not increase its expression of the phagocytic marker ED1 but exhibited high levels of triggering receptor expressed on myeloid cells-2 (TREM-2), associated with alternative microglia activation. A minor portion of the SVZ Mac-1+ cells originated from the blood early after stroke, but this macrophage population became much more substantial at later stages. Almost 80% reduction of Mac-1-expressing microglia, caused by Mac-1 saporin delivered just before and at 1week after MCAO, did not alter the numbers of newly formed neuroblasts in the striatum or their migratory distance. These findings indicate that the Mac-1-expressing microglia in the SVZ do not play a major role either for the number of neuroblasts which exit the SVZ or their migration in the striatum early following stroke.}},
author = {{Heldmann, Ursula and Mine, Yutaka and Kokaia, Zaal and Ekdahl Clementson, Christine and Lindvall, Olle}},
issn = {{0014-4886}},
language = {{eng}},
pages = {{391--398}},
publisher = {{Academic Press}},
series = {{Experimental Neurology}},
title = {{Selective depletion of Mac-1-expressing microglia in rat subventricular zone does not alter neurogenic response early after stroke.}},
url = {{https://lup.lub.lu.se/search/files/1331179/1897731.pdf}},
doi = {{10.1016/j.expneurol.2011.03.005}},
volume = {{229}},
year = {{2011}},
}