Abstract | BACKGROUND: METHODOLOGY/PRINCIPAL FINDINGS: We subjected GFAP(-/-)Vim(-/-) and wild-type mice to unilateral hypoxia- ischemia (HI) at postnatal day 9 (P9). Bromodeoxyuridine ( BrdU; 25 mg/kg) was injected intraperitoneally twice daily from P9 to P12. On P12 and P31, the animals were perfused intracardially. Immunohistochemistry with MAP-2, BrdU, NeuN, and S100 antibodies was performed on coronal sections. We found no difference in the hemisphere or infarct volume between GFAP(-/-)Vim(-/-) and wild-type mice at P12 and P31, i.e. 3 and 22 days after HI. At P31, the number of NeuN(+) neurons in the ischemic and contralateral hemisphere was comparable between GFAP(-/-)Vim(-/-) and wild-type mice. In wild-type mice, the number of S100(+) astrocytes was lower in the ipsilateral compared to contralateral hemisphere (65.0+/-50.1 vs. 85.6+/-34.0, p<0.05). In the GFAP(-/-)Vim(-/-) mice, the number of S100(+) astrocytes did not differ between the ischemic and contralateral hemisphere at P31. At P31, GFAP(-/-)Vim(-/-) mice showed an increase in NeuN(+) BrdU(+) (surviving newly born) neurons in the ischemic cortex compared to wild-type mice (6.7+/-7.7; n = 29 versus 2.9+/-3.6; n = 28, respectively, p<0.05), but a comparable number of S100(+) BrdU(+) (surviving newly born) astrocytes. CONCLUSIONS/SIGNIFICANCE: Our results suggest that attenuation of reactive gliosis in the developing brain does not affect the hemisphere or infarct volume after HI, but increases the number of surviving newborn neurons.
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Authors | Katarina Järlestedt, Catherine I Rousset, Maryam Faiz, Ulrika Wilhelmsson, Anders Ståhlberg, Hana Sourkova, Marcela Pekna, Carina Mallard, Henrik Hagberg, Milos Pekny |
Journal | PloS one
(PLoS One)
Vol. 5
Issue 4
Pg. e10397
(Apr 28 2010)
ISSN: 1932-6203 [Electronic] United States |
PMID | 20442854
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Glial Fibrillary Acidic Protein
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Topics |
- Animals
- Animals, Newborn
- Astrocytes
- Brain Infarction
(pathology)
- Cell Survival
- Glial Fibrillary Acidic Protein
(deficiency)
- Gliosis
(pathology)
- Hypoxia-Ischemia, Brain
(pathology)
- Mice
- Mice, Knockout
- Neurons
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