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Subarachnoid hemorrhage induces reactive gliosis and brain injury
Author(s) -
Murakami Kentaro,
Dumont Travis,
Tranmer Bruce I.,
Wellman George C.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.708.12
Subject(s) - gliosis , glial fibrillary acidic protein , pathology , subarachnoid hemorrhage , medicine , astrocyte , neuroscience , immunostaining , biology , immunohistochemistry , central nervous system
A wide range of CNS pathologies are known to induce reactive gliosis, including head trauma and injury, ischemic stroke, brain tumors and neurodegenerative diseases. Little is known, however, regarding the development of reactive gliosis following subarachnoid hemorrhage (SAH). The goals of this study are to characterize reactive gliosis following SAH and to determine the cellular basis of this phenomenon. Reactive gliosis was examined by the following criteria: (1) astroglial hypertrophy (detected by increased immunostaining of glial fibrillary acidic protein), (2) dedifferentiation of astrocytes (detected by re‐expression of nestin) and (3) increased metabolism of astrocytes (monitored by enhanced S‐100B production). Our results demonstrate that brain stem and cortex obtained from a rabbit SAH model exhibit these characteristics of reactive gliosis. As astrocytes have been shown to play a critical role in cerebral blood microcirculation, reactive gliosis following SAH could have a significant impact on the ability of astrocytes to communicate vasodilatory signals to parenchymal arterioles in response to neuronal activity. This work was supported by the Totman Medical Research Trust Fund, the Peter Martin Brain Aneurysm Endowment, AHA and the NIH (R20 RR16435 & R01 HL078983).