Journal
EXPERIMENTAL NEUROLOGY
Volume 269, Issue -, Pages 75-89Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2015.03.018
Keywords
CNS damage; Subependymal Zone; Subventricular Zone; Vascular Niche; Platelets; Neural Stem / Progenitor Cells; Cell Survival
Categories
Funding
- State Government of Salzburg (Austria)
- German Federal Ministry of Education and Research (BMBF) [01GN0978]
- foundation Propter Homines (Liechtenstein), through European Union [HEALTH-F2-2011-278850, HEALTH-F2-2011-279288]
- BBSRC UK [BB/I013210/1]
- Paracelsus Medical University PMU-FFF [L-12/01/001-RIV, 2058]
- FWF Special Research Program (SFB) [F4413-B23]
- Biotechnology and Biological Sciences Research Council [BB/I013210/1] Funding Source: researchfish
- BBSRC [BB/I013210/1] Funding Source: UKRI
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The presence of neural stem/progenitor cells (NSPCs) in specific areas of the central nervous system (CNS) supports tissue maintenance as well as regeneration. The subependymal zone (SEZ), located at the lateral ventricle's wall, represents a niche for NSPCs and in response to stroke or demyelination becomes activated with progenitors migrating towards the lesion and differentiating into neurons and glia. The mechanisms that underlie this phenomenon remain largely unknown. The vascular niche and in particular blood-derived elements such as platelets, has been shown to contribute to CNS regeneration in different pathological conditions. Indeed, intracerebroventricularly administrated platelet lysate (PL) stimulates angiogenesis, neurogenesis and neuroprotection in the damaged CNS. Here, we explored the presence of platelets in the activated SEZ after a focal demyelinating lesion in the corpus callosum of mice and we studied the effects of PL on proliferating SEZ-derived NSPCs in vitro. We showed that the lesion-induced increase in the size of the SEZ and in the number of proliferating SEZ-resident NSPCs correlates with the accumulation of platelets specifically along the activated SEZ vasculature. Expanding on this finding, we demonstrated that exposure of NSPCs to PL in vitro led to increased numbers of cells by enhanced cell survival and reduced apoptosis without differences in proliferation and in the differentiation potential of NSPCs. Finally, we demonstrate that the accumulation of platelets within the SEZ is spatially correlated with reduced numbers of apoptotic cells when compared to other periventricular areas. In conclusion, our results show that platelet-derived compounds specifically promote SEZ-derived NSPC survival and suggest that platelets might contribute to the enlargement of the pool of SEZ NSPCs that are available for CNS repair in response to injury. (C) 2015 Elsevier Inc All rights reserved.
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