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Proinflammatory Cytokine Effects on Mesenchymal Stem Cell Therapy for the Ischemic Heart
Aaron M. Abarbanell, MD, Arthur C. Coffey, MD, John W. Fehrenbacher, MD, Daniel J. Beckman, MD, Jeremy L. Herrmann, MD, Brent Weil, MD, Daniel R. Meldrum, MD The Annals of Thoracic Surgery Volume 88, Issue 3, Pages (September 2009) DOI: /j.athoracsur Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions
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Fig 1 Selected cytokines and associated pathways that affect mesenchymal stem cell (MSC) function. Multiple cytokines alter MSC function. The known receptors and pathways are shown. Based on the known research, it is likely that crosstalk exists at multiple intracellular levels. (HGF = hepatocyte growth factor; HMGB1 = high mobility group box 1; IGF-1 = insulin-like growth factor-1; MET = mesenchymal-epithelial transition factor receptor; NF-κB = nuclear factor kappa-B; RAGE = receptor for advanced glycation end products; TGF-β1 = transforming growth factor-beta 1; TLR = toll-like receptor; TNF = tumor necrosis factor; TNFR1 = tumor necrosis factor receptor 1; TNFR2 = tumor necrosis factor receptor 2; VEGF = vascular endothelial growth factor.) The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions
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Fig 2 Schematic of three targets that modulate the effects of cytokines on mesenchymal stem cell (MSC) function. Cytokines affect MSC function. The effects of cytokine stimuli can be augmented or repressed at the receptor level or at the intracellular level in MSCs. Alternatively, MSCs can be modified to overexpress cytokines that may affect MSC function in vivo. The Annals of Thoracic Surgery , DOI: ( /j.athoracsur ) Copyright © 2009 The Society of Thoracic Surgeons Terms and Conditions
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