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Tumor Necrosis Factor α Regulates Endothelial Progenitor Cell Migration via CADM1 and NF-kB.
Prisco, Anthony R; Hoffmann, Brian R; Kaczorowski, Catherine C; McDermott-Roe, Chris; Stodola, Timothy J; Exner, Eric C; Greene, Andrew S.
Afiliación
  • Prisco AR; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.
  • Hoffmann BR; Medical College of Wisconsin, Biotechnology and Bioengineering Center, Milwaukee, WI, USA.
  • Kaczorowski CC; Medical College of Wisconsin, Biotechnology and Bioengineering Center, Milwaukee, WI, USA.
  • McDermott-Roe C; Department of Medicine, Division of Cardiology, Medical College of Wisconsin, Milwaukee, WI, USA.
  • Stodola TJ; Medical College of Wisconsin, Cardiovascular Center, Milwaukee, WI, USA.
  • Exner EC; Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, Memphis, TN, USA.
  • Greene AS; Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Stem Cells ; 34(7): 1922-33, 2016 07.
Article en En | MEDLINE | ID: mdl-26867147
Shortly after the discovery of endothelial progenitor cells (EPCs) in 1997, many clinical trials were conducted using EPCs as a cellular based therapy with the goal of restoring damaged organ function by inducing growth of new blood vessels (angiogenesis). Results were disappointing, largely because the cellular and molecular mechanisms of EPC-induced angiogenesis were not clearly understood. Following injection, EPCs must migrate to the target tissue and engraft prior to induction of angiogenesis. In this study EPC migration was investigated in response to tumor necrosis factor α (TNFα), a pro-inflammatory cytokine, to test the hypothesis that organ damage observed in ischemic diseases induces an inflammatory signal that is important for EPC homing. In this study, EPC migration and incorporation were modeled in vitro using a coculture assay where TNFα treated EPCs were tracked while migrating toward vessel-like structures. It was found that TNFα treatment of EPCs increased migration and incorporation into vessel-like structures. Using a combination of genomic and proteomic approaches, NF-kB mediated upregulation of CADM1 was identified as a mechanism of TNFα induced migration. Inhibition of NF-kB or CADM1 significantly decreased migration of EPCs in vitro suggesting a role for TNFα signaling in EPC homing during tissue repair. Stem Cells 2016;34:1922-1933.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / FN-kappa B / Factor de Necrosis Tumoral alfa / Células Progenitoras Endoteliales / Molécula 1 de Adhesión Celular Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Stem Cells Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Movimiento Celular / FN-kappa B / Factor de Necrosis Tumoral alfa / Células Progenitoras Endoteliales / Molécula 1 de Adhesión Celular Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Stem Cells Año: 2016 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido