4.7 Article

Effects of Neural Progenitor Cells on Sensorimotor Recovery and Endogenous Repair Mechanisms After Photothrombotic Stroke

Journal

STROKE
Volume 42, Issue 6, Pages 1757-1763

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/STROKEAHA.110.599282

Keywords

neural progenitor cells; recovery; stroke

Funding

  1. Innovative Medizinische Forschung (IMF) of the Medical Faculty of the University of Munster [MI 120815]
  2. Bundesministerium fur Bildung und Forschung (BMBF) [01GN0980]
  3. UNIST
  4. ministry of Education, Science, and Technology [2010-0020277]
  5. Science Research Center Fund, Republic of Korea [2010-0029436]
  6. National Research Foundation of Korea [2010-0020277, 2010-0029436] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Background and Purpose-Intravenous neural progenitor cell (NPC) treatment was shown to improve functional recovery after experimental stroke. The underlying mechanisms, however, are not completely understood so far. Here, we investigated the effects of systemic NPC transplantation on endogenous neurogenesis and dendritic plasticity of host neurons. Methods-Twenty-four hours after photothrombotic ischemia, adult rats received either 5 million NPC or placebo intravenously. Behavioral tests were performed weekly up to 4 weeks after ischemia. Endogenous neurogenesis, dendritic length, and dendritic branching of cortical pyramid cells and microglial activation were quantified. Results-NPC treatment led to a significantly improved sensorimotor function measured by the adhesive removal test. The dendritic length and the amount of branch points were significantly increased after NPC transplantation, whereas endogenous neurogenesis was decreased compared to placebo therapy. Decreased endogenous neurogenesis was associated with an increased number of activated microglial cells. Conclusions-Our findings suggest that an increased dendritic plasticity might be the structural basis of NPC-induced functional recovery. The decreased endogenous neurogenesis after NPC treatment seems to be mediated by microglial activation. (Stroke. 2011; 42: 1757-1763.)

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