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Absence of glial fibrillary acidic protein and vimentin prevents hypertrophy of astrocytic processes and improves post-traumatic regeneration

Artikel i vetenskaplig tidskrift
Författare Ulrika Wilhelmsson
Lizhen Li
Marcela Pekna
Claes-Henric Berthold
Sofia Blom
Camilla Eliasson
O. Renner
E. Bushong
M. Ellisman
T. E. Morgan
Milos Pekny
Publicerad i J Neurosci
Volym 24
Nummer/häfte 21
Sidor 5016-21
ISSN 1529-2401 (Electronic)
Publiceringsår 2004
Publicerad vid Institutionen för medicinsk och fysiologisk kemi
Institutionen för anatomi och cellbiologi
Sidor 5016-21
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Astrocytes/*metabolism/ultrastructure, Brain Injuries/pathology/*physiopathology, Cells, Cultured, Cytoplasm/ultrastructure, Entorhinal Cortex/injuries, Glial Fibrillary Acidic Protein/*metabolism, Glutamate-Ammonia Ligase/metabolism, Hippocampus/*metabolism/*ultrastructure, Hypertrophy/metabolism/pathology/prevention & control, Mice, Mice, Inbred C57BL, Nerve Regeneration/*physiology, Receptor, Endothelin B/metabolism, Up-Regulation, Vimentin/*metabolism
Ämneskategorier Neurobiologi

Sammanfattning

The regenerative capacity of the CNS is extremely limited. The reason for this is unclear, but glial cell involvement has been suspected, and oligodendrocytes have been implicated as inhibitors of neuroregeneration (Chen et al., 2000, GrandPre et al., 2000; Fournier et al., 2001). The role of astrocytes in this process was proposed but remains incompletely understood (Silver and Miller, 2004). Astrocyte activation (reactive gliosis) accompanies neurotrauma, stroke, neurodegenerative diseases, or tumors. Two prominent hallmarks of reactive gliosis are hypertrophy of astrocytic processes and upregulation of intermediate filaments. Using the entorhinal cortex lesion model in mice, we found that reactive astrocytes devoid of the intermediate filament proteins glial fibrillary acidic protein and vimentin (GFAP-/-Vim-/-), and consequently lacking intermediate filaments (Colucci-Guyon et al., 1994; Pekny et al., 1995; Eliasson et al., 1999), showed only a limited hypertrophy of cell processes. Instead, many processes were shorter and not straight, albeit the volume of neuropil reached by a single astrocyte was the same as in wild-type mice. This was accompanied by remarkable synaptic regeneration in the hippocampus. On a molecular level, GFAP-/-Vim-/- reactive astrocytes could not upregulate endothelin B receptors, suggesting that the upregulation is intermediate filament dependent. These findings show a novel role for intermediate filaments in astrocytes and implicate reactive astrocytes as potent inhibitors of neuroregeneration.

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