Prion protein and its ligand stress inducible protein 1 regulate astrocyte development

Prion protein (PrPC) interaction with stress inducible protein 1 (STI1) mediates neuronal survival and differentiation. However, the function of PrPC in astrocytes has not been approached. In this study, we show that STI1 prevents cell death in wild‐type astrocytes in a protein kinase A‐dependent ma...

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Published in:Glia 2009-10, Vol.57 (13), p.1439-1449
Main Authors: Arantes, Camila, Nomizo, Regina, Lopes, Marilene H., Hajj, Glaucia N. M., Lima, Flavia R. S., Martins, Vilma R.
Format: Article
Language:English
Subjects:
Animals
astrocyte
Astrocytes - cytology
Astrocytes - physiology
Brain - physiology
Cell Differentiation - physiology
Cell Proliferation
Cell Survival - physiology
Cells, Cultured
Cyclic AMP-Dependent Protein Kinases - metabolism
differentiation
Glial Fibrillary Acidic Protein - metabolism
Heat-Shock Proteins - metabolism
Intermediate Filament Proteins - metabolism
MAP Kinase Signaling System
Mice
Mice, Knockout
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Models, Neurological
Nerve Tissue Proteins - metabolism
Nestin
proliferation
Protein Kinase C - metabolism
PrPC
PrPC Proteins - genetics
PrPC Proteins - metabolism
Recombinant Proteins - metabolism
Signal Transduction
STI1
survival
Vimentin - metabolism
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Summary:Prion protein (PrPC) interaction with stress inducible protein 1 (STI1) mediates neuronal survival and differentiation. However, the function of PrPC in astrocytes has not been approached. In this study, we show that STI1 prevents cell death in wild‐type astrocytes in a protein kinase A‐dependent manner, whereas PrPC‐null astrocytes were not affected by STI1 treatment. At embryonic day 17, cultured astrocytes and brain extracts derived from PrPC‐null mice showed a reduced expression of glial fibrillary acidic protein (GFAP) and increased vimentin and nestin expression when compared with wild‐type, suggesting a slower rate of astrocyte maturation in PrPC‐null animals. Furthermore, PrPC‐null astrocytes treated with STI1 did not differentiate from a flat to a process‐bearing morphology, as did wild‐type astrocytes. Remarkably, STI1 inhibited proliferation of both wild‐type and PrPC‐null astrocytes in a protein kinase C‐dependent manner. Taken together, our data show that PrPC and STI1 are essential to astrocyte development and act through distinct signaling pathways. © 2009 Wiley‐Liss, Inc.
ISSN:0894-1491
1098-1136
DOI:10.1002/glia.20861