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Protective role of reactive astrocytes in brain ischemia.

Artikel i vetenskaplig tidskrift
Författare Lizhen Li
Andrea Lundkvist
Daniel Andersson
Ulrika Wilhelmsson
Nobuo Nagai
Andrea C Pardo
Christina Nodin
Anders Ståhlberg
Karina Aprico
Kerstin Larsson
Takeshi Yabe
Lieve Moons
Andrew Fotheringham
Ioan Davies
Peter Carmeliet
Joan P Schwartz
Marcela Pekna
Mikael Kubista
Fredrik Blomstrand
Nicholas Maragakis
Michael Nilsson
Milos Pekny
Publicerad i Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
Volym 28
Nummer/häfte 3
Sidor 468-81
ISSN 0271-678X
Publiceringsår 2008
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 468-81
Språk en
Länkar dx.doi.org/10.1038/sj.jcbfm.9600546
Ämnesord Animals, Astrocytes, pathology, physiology, Brain Ischemia, metabolism, pathology, Gap Junctions, Glial Fibrillary Acidic Protein, deficiency, Glutamic Acid, metabolism, Mice, Mice, Knockout, Middle Cerebral Artery, Plasminogen Activator Inhibitor 1, genetics, Receptor, Endothelin B, analysis, Vimentin, deficiency
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Reactive astrocytes are thought to protect the penumbra during brain ischemia, but direct evidence has been lacking due to the absence of suitable experimental models. Previously, we generated mice deficient in two intermediate filament (IF) proteins, glial fibrillary acidic protein (GFAP) and vimentin, whose upregulation is the hallmark of reactive astrocytes. GFAP(-/-)Vim(-/-) mice exhibit attenuated posttraumatic reactive gliosis, improved integration of neural grafts, and posttraumatic regeneration. Seven days after middle cerebral artery (MCA) transection, infarct volume was 210 to 350% higher in GFAP(-/-)Vim(-/-) than in wild-type (WT) mice; GFAP(-/-), Vim(-/-) and WT mice had the same infarct volume. Endothelin B receptor (ET(B)R) immunoreactivity was strong on cultured astrocytes and reactive astrocytes around infarct in WT mice but undetectable in GFAP(-/-)Vim(-/-) astrocytes. In WT astrocytes, ET(B)R colocalized extensively with bundles of IFs. GFAP(-/-)Vim(-/-) astrocytes showed attenuated endothelin-3-induced blockage of gap junctions. Total and glutamate transporter-1 (GLT-1)-mediated glutamate transport was lower in GFAP(-/-)Vim(-/-) than in WT mice. DNA array analysis and quantitative real-time PCR showed downregulation of plasminogen activator inhibitor-1 (PAI-1), an inhibitor of tissue plasminogen activator. Thus, reactive astrocytes have a protective role in brain ischemia, and the absence of astrocyte IFs is linked to changes in glutamate transport, ET(B)R-mediated control of gap junctions, and PAI-1 expression.

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