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The bone morphogenetic protein type Ib receptor is a major mediator of glial differentiation and cell survival in adult hippocampal progenitor cell culture.

Artikel i vetenskaplig tidskrift
Författare Anke Brederlau
Roland Faigle
Muna Elmi
A. Zarebski
Sara Sjöberg
M. Fujii
K. Miyazono
Keiko Funa
Publicerad i Molecular biology of the cell
Volym 15
Nummer/häfte 8
Sidor 3863-75
ISSN 1059-1524
Publiceringsår 2004
Publicerad vid Institutionen för anatomi och cellbiologi
Sidor 3863-75
Språk en
Länkar dx.doi.org/10.1091/mbc.E03-08-0584
Ämnesord Adenoviridae, genetics, Animals, Bone Morphogenetic Protein Receptors, Type I, Bone Morphogenetic Proteins, antagonists & inhibitors, genetics, physiology, Carrier Proteins, Cell Death, genetics, physiology, Cell Differentiation, genetics, physiology, Cells, Cultured, Gene Expression, genetics, Glial Fibrillary Acidic Protein, analysis, genetics, metabolism, Hippocampus, cytology, Ligands, Mutation, genetics, Neuroglia, cytology, metabolism, Protein-Serine-Threonine Kinases, analysis, genetics, physiology, Proteins, genetics, metabolism, pharmacology, RNA, Messenger, analysis, metabolism, Rats, Receptors, Growth Factor, analysis, genetics, physiology, Stem Cells, cytology, metabolism
Ämneskategorier Cell- och molekylärbiologi

Sammanfattning

Bone morphogenetic proteins (BMPs) act as growth regulators and inducers of differentiation. They transduce their signal via three different type I receptors, termed activin receptor-like kinase 2 (Alk2), Alk3, or bone morphogenetic protein receptor Ia (BMPRIa) and Alk6 or BMPRIb. Little is known about functional differences between the three type I receptors. Here, we have investigated consequences of constitutively active (ca) and dominant negative (dn) type I receptor overexpression in adult-derived hippocampal progenitor cells (AHPs). The dn receptors have a nonfunctional intracellular but functional extracellular domain. They thus trap BMPs that are endogenously produced by AHPs. We found that effects obtained by overexpression of dnAlk2 and dnAlk6 were similar, suggesting similar ligand binding patterns for these receptors. Thus, cell survival was decreased, glial fibrillary acidic protein (GFAP) expression was reduced, whereas the number of oligodendrocytes increased. No effect on neuronal differentiation was seen. Whereas the expression of Alk2 and Alk3 mRNA remained unchanged, the Alk6 mRNA was induced after impaired BMP signaling. After dnAlk3 overexpression, cell survival and astroglial differentiation increased in parallel to augmented Alk6 receptor signaling. We conclude that endogenous BMPs mediate cell survival, astroglial differentiation and the suppression of oligodendrocytic cell fate mainly via the Alk6 receptor in AHP culture.

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