10.1111/jcmm.12298
https://zenodo.org/records/11519
oai:zenodo.org:11519
Kandasamy, Mahesh
Mahesh
Kandasamy
Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria and Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University, Salzburg, Austria
Lehner, Bernadette
Bernadette
Lehner
Department of Neurology, University Hospital Regensburg, Regensburg, Germany
Kraus, Sabrina
Sabrina
Kraus
Department of Experimental Ophthalmology, University of Regensburg, Regensburg, Germany
Ramm Sander, Paul
Paul
Ramm Sander
Department of Neurology, University Hospital Regensburg, Regensburg, Germany and Institute of Biophysics and Physical Biochemistry, University of Regensburg, Regensburg, Germany
Marschallinger, Julia
Julia
Marschallinger
Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria and Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University, Salzburg, Austria
Rivera, Francisco J.
Francisco J.
Rivera
Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria and Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University, Salzburg, Austria
Trümbach, Dietrich
Dietrich
Trümbach
Institute of Developmental Genetics, Helmholtz Centre Munich, German Research Centre for Environmental Health (GmbH), Technical University Munich, Neuherberg, Germany
Ueberham, Uwe
Uwe
Ueberham
Paul Flechsig Institute for Brain Research, Department of Neuroanatomy, University of Leipzig, Leipzig, Germany
Reitsamer, Herbert A.
Herbert A.
Reitsamer
Department of Ophthalmology, SALK, Paracelsus Medical University, Salzburg, Austria
Strauss, Olaf
Olaf
Strauss
Department of Experimental Ophthalmology, University of Regensburg, Regensburg, Germany
Bogdahn, Ulrich
Ulrich
Bogdahn
Department of Neurology, University Hospital Regensburg, Regensburg, Germany
Couillard-Despres, Sebastien
Sebastien
Couillard-Despres
Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University, Salzburg, Austria and Institute of Experimental Neuroregeneration, Paracelsus Medical University, Salzburg, Austria
Aigner, Ludwig
Ludwig
Aigner
Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria and Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University, Salzburg, Austria
TGF-beta signalling in the adult neurogenic niche promotes stem cell quiescence as well as generation of new neurons.
Zenodo
2014
TGF-b1
Smad2
stem cells
cell cycle
doublecortin
differentiation
2014-04-30
https://zenodo.org/communities/inmind
https://zenodo.org/communities/eu
Creative Commons Attribution 4.0 International
Members of the transforming growth factor (TGF)-b family govern a wide range of mechanisms in brain development and in the adult, in particular neuronal/glial differentiation and survival, but also cell cycle regulation and neural stem cell maintenance. This clearly created some discrepancies in the field with some studies favouring neuronal differentiation/survival of progenitors and others favouring cell cycle exit and neural stem cell quiescence/maintenance. Here, we provide a unifying hypothesis claiming that through its regulation of neural progenitor cell (NPC) proliferation, TGF-b signalling might be responsible for (i) maintaining stem cells in a quiescent stage, and (ii) promoting survival of newly generated neurons and their functional differentiation. Therefore, we performed a detailed histological analysis of TGF-b1 signalling in the hippocampal neural stem cell niche of a transgenic mouse that was previously generated to express TGF-b1 under a tetracycline regulatable Ca-Calmodulin kinase promoter. We also analysed NPC proliferation, quiescence, neuronal survival and differentiation in relation to elevated levels of TGF-b1 in vitro and in vivo conditions. Finally, we performed a gene expression profiling to identify the targets of TGF-b1 signalling in adult NPCs. The results demonstrate that TGF-b1 promotes stem cell quiescence on one side, but also neuronal survival on the other side. Thus, considering the elevated levels of TGF-b1 in ageing and neurodegenerative diseases, TGF-b1 signalling presents a molecular target for future interventions in such conditions.
European Commission
10.13039/501100000780
278850
Imaging of Neuroinflammation in Neurodegenerative Diseases