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      iNSC suppress macrophage-induced inflammation by repressing COX-2.

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          Abstract

          Brain inflammation causes cell damage and death in diseases such as Alzheimer's and Parkinson's. In this study, we investigated whether early induced neural stem cells (iNSCs) could protect against cell death after treatment with THP1-derived macrophages. We developed an inflammatory model system with THP1-derived macrophages and cortical neuronal cells and investigated the therapeutic efficacy of iNSC against macrophage-induced inflammation in this model. Apoptosis was confirmed by double immunocytochemistry with NeuN and 4',6-diamidino-2-phenylindole using terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP-biotin nick-end labeling. Cortical neuronal cells cultured with iNSCs exhibited fewer apoptotic cells than did cultures without iNSCs. The levels of inflammatory cytokines and vascular endothelial growth factor (VEGF) were analyzed by enzyme-linked immunosorbent assay. Cells cultured with iNSCs had lower levels of inflammatory cytokines and higher VEGF levels than those cultured without iNSCs. Western blot analysis for cyclooxygenase-2 (COX-2) showed a significantly lower level of COX-2 in cells cultured with iNSCs than in those cultured without iNSCs. Thus, early iNSCs administration reduced inflammation associated with neurological recovery, and this effect is mediated by COX-2 regulation. Our results suggest that iNSCs have potential therapeutic relevance, because they display strong anti-inflammatory functions that promote neuroprotection thorough the inflammatory response.

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          Author and article information

          Journal
          In Vitro Cell. Dev. Biol. Anim.
          In vitro cellular & developmental biology. Animal
          1543-706X
          1071-2690
          Feb 2015
          : 51
          : 2
          Affiliations
          [1 ] Department of Neurosurgery, College of Medicine, Korea University, Seoul, Korea.
          Article
          10.1007/s11626-014-9816-4
          25248435
          76123b3c-c327-4e67-a05a-13b189748c7d
          History

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