期刊
PLOS ONE
卷 5, 期 4, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0010397
关键词
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资金
- Swedish Research Council [11548, 20116, 09455, 14185]
- Medical Research Council (United Kingdom) [P19381]
- LUA/ALF Gothenburg
- Region of Vastra Gotaland
- Ragnar and Torsten Soderberg's Foundations
- Hjarnfonden
- Edith Jacobsson's Foundation
- John and Brit Wennerstrom's Foundation
- W. and M. Lundgren's Foundation
- A. and U. Amlov's Foundation
- Free Mason Foundation
- Swedish Stroke Foundation
- [ALFGBG7592]
- [ALFGBG11267]
- [ALFGBG2863]
- Austrian Science Fund (FWF) [P19381] Funding Source: Austrian Science Fund (FWF)
- Action Medical Research [1764] Funding Source: researchfish
- Medical Research Council [G0802853] Funding Source: researchfish
- MRC [G0802853] Funding Source: UKRI
Background: Astroglial cells are activated following injury and up-regulate the expression of the intermediate filament proteins glial fibrillary acidic protein (GFAP) and vimentin. Adult mice lacking the intermediate filament proteins GFAP and vimentin (GFAP(-/-) Vim(-/-)) show attenuated reactive gliosis, reduced glial scar formation and improved regeneration of neuronal synapses after neurotrauma. GFAP(-/-) Vim(-/-) mice exhibit larger brain infarcts after middle cerebral artery occlusion suggesting protective role of reactive gliosis after adult focal brain ischemia. However, the role of astrocyte activation and reactive gliosis in the injured developing brain is unknown. 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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