• Medientyp: E-Artikel
  • Titel: Endothelial Progenitor Cells Conditioned Medium Supports Number of GABAergic Neurons and Exerts Neuroprotection in Cultured Striatal Neuronal Progenitor Cells
  • Beteiligte: Santo, Stefano Di; Seiler, Stefanie; Andres, Robert; Widmer, Hans Rudolf
  • Erschienen: SAGE Publications, 2019
  • Erschienen in: Cell Transplantation, 28 (2019) 4, Seite 367-378
  • Sprache: Englisch
  • DOI: 10.1177/0963689719835192
  • ISSN: 0963-6897; 1555-3892
  • Schlagwörter: Transplantation ; Cell Biology ; Biomedical Engineering
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  • Beschreibung: <jats:p> There is growing evidence that stem and progenitor cells exert regenerative actions by means of paracrine factors. In line with these notions, we recently demonstrated that endothelial progenitor cell (EPC)-derived conditioned medium (EPC-CM) substantially increased viability of brain microvascular cells. In the present study, we aimed at investigating whether EPC-CM supports cell survival of cultured striatal progenitor cells. For that purpose, primary cultures from fetal rat embryonic (E14) ganglionic eminence were prepared and grown for 7 days in vitro (DIV). EPC-CM was administered from DIV5–7. Treatment of the striatal cultures with EPC-CM resulted in significantly increased densities of GABA-immunoreactive (-ir) neurons. Inhibition of mitogen-activated protein kinase and phosphatidylinositol-3-kinase, but not of the ROCK pathway, significantly attenuated the EPC-CM induced increase in GABA-ir cell densities. Similar results were observed when EPC-CM was subjected to proteolytic digestion and lipid extraction. Furthermore, inhibition of translation abolished the EPC-CM induced effects. Importantly, EPC-CM displayed neuroprotection against 3-nitropropionic acid induced toxicity. These findings demonstrate that EPC-derived paracrine factors substantially promote survival and/or differentiation of cultured striatal progenitor cells involving both proteinaceous factors and lipidic factors. In sum, EPC-CM constituents might lead to a novel cell-free therapeutic strategy to challenge neuronal degeneration. </jats:p>
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