Lesion-induced accumulation of platelets promotes survival of adult neural stem / progenitor cells.

Exp Neurol

Wellcome Trust and MRC Cambridge Stem Cell Institute & Department of Veterinary Medicine, University of Cambridge, Cambridge, United Kingdom; Institute of Molecular Regenerative Medicine, Paracelsus Medical University Salzburg, Salzburg, Austria; Spinal Cord Injury and Tissue Regeneration Center Salzburg, Paracelsus Medical University Salzburg, Salzburg, Austria. Electronic address:

Published: July 2015

AI Article Synopsis

  • Neural stem/progenitor cells (NSPCs) in the subependymal zone (SEZ) of the central nervous system (CNS) can activate and migrate to repair damage caused by stroke or demyelination, although the exact mechanisms behind this are still unclear.
  • The research found that after a demyelinating lesion in mice, platelets accumulated in the SEZ, which correlated with increased NSPC proliferation and survival, indicating a possible role for platelets in promoting CNS regeneration.
  • Exposure to platelet lysate (PL) in vitro not only boosted NSPC cell survival and reduced apoptosis but also implied that platelet-derived compounds can help expand the population of NSPCs available for repairing CNS injuries.

Article Abstract

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.

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http://dx.doi.org/10.1016/j.expneurol.2015.03.018DOI Listing

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