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hmscs, pubmed, cells, cell, culture, article, nad, expansion, stem, google, scholar, fig, cas, mitochondrial, senescence, metabolic, human, mesenchymal, central, metabolism, cellular, passage, replicative, increased, sirt, activity, level, vitro, nadnadh, redox, cycle, late, results, hfbs, hmsc, levels, analysis, exhibit, decreased, senescent, intracellular, homeostasis, autophagy, supplementary, min, nature, aging, atp, nadh, pathways,

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nature portfolio steroid-resistant graft-versus-host disease privacy policy ovarian research advertising research participants nature 509 nature 529 nature 543 nature reduced sa-β-gal activity author information authors glycolysis inhibitor 2-deoxy-d-glucose reprints fatty acid beta-oxidation mesenchymal stromal/stem cells open square amp-activated protein kinase sa-β-gal activity nutrient-enriched culture environment full size image sa-β-gal staining deficiency-induced hepatic lipotoxicity original author pi3k-akt signaling pathway fitc-conjugated secondary antibody nad + precursor nicotinamide increases thermo scientific nad+/nadh redox balance urh1/pnp1/meu1 pathways gas chromatography–mass spectrometry colony-forming unit-fibroblast 20 µm cyto-id green u-13c- labeled glucose exhibit multi-lineage differentiation nad+/nadh redox cycle santa cruz biotechnology anchored oligo-dt primers small-size fragmented morphology colony-forming unit-fibroblasts data availability statement cyclic adp-ribose synthases exhibit culture-induced senescence long-term culture expansion key nad+-dependent enzymes nad+-dependent sirtuin enzymes increased tail/body length cellular nad + /nadh balance including lineage-specific differentiation 20 µl n-methyl-n

Questions {❓}

• Fibroblasts and mesenchymal stem cells: two sides of the same coin?
• Metabolism in human mesenchymal stromal cells: a missing link between hMSC biomanufacturing and therapy?
• Mitochondria–a nexus for aging, calorie restriction, and sirtuins?
• Reduced nicotinamide adenine dinucleotide phosphate in redox balance and diseases: a friend or foe?
• Replicative senescence: an old lives’ tale?
• The mesenchymal stromal cells dilemma–does a negative phase III trial of random donor mesenchymal stromal cells in steroid-resistant graft-versus-host disease represent a death knell or a bump in the road?

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         description:Human mesenchymal stem cells (hMSCs) promote endogenous tissue regeneration and have become a promising candidate for cell therapy. However, in vitro culture expansion of hMSCs induces a rapid decline of stem cell properties through replicative senescence. Here, we characterize metabolic profiles of hMSCs during expansion. We show that alterations of cellular nicotinamide adenine dinucleotide (NAD + /NADH) redox balance and activity of the Sirtuin (Sirt) family enzymes regulate cellular senescence of hMSCs. Treatment with NAD + precursor nicotinamide increases the intracellular NAD + level and re-balances the NAD + /NADH ratio, with enhanced Sirt-1 activity in hMSCs at high passage, partially restores mitochondrial fitness and rejuvenates senescent hMSCs. By contrast, human fibroblasts exhibit limited senescence as their cellular NAD + /NADH balance is comparatively stable during expansion. These results indicate a potential metabolic and redox connection to replicative senescence in adult stem cells and identify NAD + as a metabolic regulator that distinguishes stem cells from mature cells. This study also suggests potential strategies to maintain cellular homeostasis of hMSCs in clinical applications. Yuan et al. characterise metabolic profiles of human mesenchymal stem cells (hMSCs) during cell expansion in culture. They find that late passage hMSCs exhibit a NAD + /NADH redox cycle imbalance and that adding NAD + precursor nicotinamide restores mitochondrial fitness and cellular homeostasis in senescent hMSCs indicating a possible route to preserve hMSC homeostasis for therapeutic use.
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      headline:NAD+/NADH redox alterations reconfigure metabolism and rejuvenate senescent human mesenchymal stem cells in vitro
      description:Human mesenchymal stem cells (hMSCs) promote endogenous tissue regeneration and have become a promising candidate for cell therapy. However, in vitro culture expansion of hMSCs induces a rapid decline of stem cell properties through replicative senescence. Here, we characterize metabolic profiles of hMSCs during expansion. We show that alterations of cellular nicotinamide adenine dinucleotide (NAD + /NADH) redox balance and activity of the Sirtuin (Sirt) family enzymes regulate cellular senescence of hMSCs. Treatment with NAD + precursor nicotinamide increases the intracellular NAD + level and re-balances the NAD + /NADH ratio, with enhanced Sirt-1 activity in hMSCs at high passage, partially restores mitochondrial fitness and rejuvenates senescent hMSCs. By contrast, human fibroblasts exhibit limited senescence as their cellular NAD + /NADH balance is comparatively stable during expansion. These results indicate a potential metabolic and redox connection to replicative senescence in adult stem cells and identify NAD + as a metabolic regulator that distinguishes stem cells from mature cells. This study also suggests potential strategies to maintain cellular homeostasis of hMSCs in clinical applications. Yuan et al. characterise metabolic profiles of human mesenchymal stem cells (hMSCs) during cell expansion in culture. They find that late passage hMSCs exhibit a NAD + /NADH redox cycle imbalance and that adding NAD + precursor nicotinamide restores mitochondrial fitness and cellular homeostasis in senescent hMSCs indicating a possible route to preserve hMSC homeostasis for therapeutic use.
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