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Journal ArticleDOI

Quantitative aspects of reactive gliosis: A review

TLDR
There are different biological mechanisms for induction and maintenance of reactive gliosis, which, depending on the kind of tissue damage, result in different expressions of the gliotic response.
Abstract
Recent studies of gliosis in a variety of animal models are reviewed. The models include brain injury, neurotoxic damage, genetic diseases and inflammatory demyelination. These studies show that reactive gliosis is not a stereotypic response, but varies widely in duration, degree of hyperplasia, and time course of expression of GFAP immunostaining, content and mRNA. We conclude that there are different biological mechanisms for induction and maintenance of reactive gliosis, which, depending on the kind of tissue damage, result in different expressions of the gliotic response.

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Citations
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Astrocytes: biology and pathology

TL;DR: Astrocyte functions in healthy CNS, mechanisms and functions of reactive astrogliosis and glial scar formation, and ways in which reactive astrocytes may cause or contribute to specific CNS disorders and lesions are reviewed.
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Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

TL;DR: Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function, and the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans.
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The glial scar and central nervous system repair

TL;DR: Deyelinated plaques in multiple sclerosis consists mostly of scar-type astrocytes and naked axons, but astroCytes inhibit the migration of both oligodendrocyte precursors and Schwann cells which must restrict their access to demyelinated axons.
Journal ArticleDOI

Reactive astrocytes: cellular and molecular cues to biological function

TL;DR: Reactive astrocytes should be considered a key element, like neurons, of a dynamic environment, thus forming with neurons a functional unit involved in homeostasis, plasticity and neurotransmission.
Journal ArticleDOI

Molecular profile of reactive astrocytes—Implications for their role in neurologic disease

TL;DR: A summary of molecules whose levels of expression differentiate activated from resting astrocytes is provided and it becomes apparent that reactive astroCytes may benefit the injured nervous system by participating in diverse biological processes.
References
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Journal ArticleDOI

Localization of the glial fibrillary acidic protein in astrocytes by immunofluorescence

TL;DR: The glial fibrillary acidic (GFA) protein, a brain specific protein extracted from severely gliosed human tissue, is not species specific; cross-reaction occurs between anti-human GFA protein antibodies and brain extracts of rabbit, guinea pig, rat and dog.
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Interleukin-1 stimulation of astroglial proliferation after brain injury.

Dana Giulian, +1 more
- 26 Apr 1985 - 
TL;DR: Findings suggest that interleukin-1, released by inflammatory cells, may promote the formation of scars by astroglia in the damaged mammalian brain.
Journal ArticleDOI

Glial fibrillary acidic protein (GFAP): the major protein of glial intermediate filaments in differentiated astrocytes.

TL;DR: The glial fibrillary acidic protein (GFA protein or GFAP) is the major protein constituent of glial intermediate filaments in differentiated fibrous and protoplasmic astrocytes of the central nervous system.
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Immunocytochemical demonstration of vimentin in astrocytes and ependymal cells of developing and adult mouse nervous system.

TL;DR: The results show that vimentin and GFA protein coexist in one cell type not only in primary cultures in vitro but also in the intact tissue in situ.
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