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Related Concept Videos

Methods of Nuclear Reprogramming01:24

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Nuclear reprogramming is a process of transforming one cell type into an unrelated cell type by epigenetic changes that alter the cell’s original gene expression pattern. Such epigenetic changes force cells to express a different set of genes, which play a significant role in inducing transformation into other cell types. Nuclear reprogramming offers applications in reproductive cloning for livestock propagation and regenerative medicine — developing patient-specific cells for...
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Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
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Introduction to Nuclear Reprogramming01:14

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Nuclear reprogramming is the process of switching gene expression of one cell type to that of another cell type, usually from a differentiated cell state to an undifferentiated cell state. Differentiation occurs during processes such as development and morphogenesis, tissue regeneration, and malignancy. Cells can also be artificially induced to reprogram their gene expression by techniques such as nuclear transfer, induced pluripotency, and cell fusion. Such techniques have many applications in...
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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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Stem cells are undifferentiated cells that divide and produce different types of cells. Ordinarily, cells that have differentiated into a specific cell type are post-mitotic—that is, they no longer divide. However, scientists have found a way to reprogram these mature cells so that they “de-differentiate” and return to an unspecialized, proliferative state. These cells are also pluripotent like embryonic stem cells—able to produce all cell types—and are therefore...
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NRF2 Orchestrates the Metabolic Shift during Induced Pluripotent Stem Cell Reprogramming.

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Understanding induced pluripotent stem cell (iPSC) reprogramming requires studying metabolic shifts. Early NRF2 activation drives the glycolytic shift, crucial for efficient iPSC generation.

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Area of Science:

  • Stem cell biology
  • Cellular metabolism
  • Molecular mechanisms of reprogramming

Background:

  • Induced pluripotent stem cells (iPSCs) hold great promise for regenerative medicine and disease modeling.
  • Current iPSC generation methods are inefficient, necessitating a deeper understanding of the underlying cellular processes.
  • Metabolic reprogramming, specifically the shift from oxidative phosphorylation to glycolysis, is a critical event during iPSC induction.

Purpose of the Study:

  • To investigate the longitudinal changes in cell signaling and transcription factor activity during human iPSC reprogramming.
  • To elucidate the metabolic mechanisms that govern the efficiency of iPSC generation.
  • To identify key transcription factors and metabolic pathways involved in the early stages of reprogramming.

Main Methods:

  • Development of a lentiviral reporter system for real-time monitoring of cellular signaling and transcription factor activity.
  • Reprogramming of human dermal fibroblasts into iPSCs.
  • Analysis of transcription factor activation (NF-κB, AP-1, NRF2, HIFα) and metabolic changes.
  • Functional assays involving inhibition of NRF2 activity via KEAP1 overexpression.

Main Results:

  • Early activation of NF-κB, AP-1, and NRF2 transcription factors precedes the peak activity of hypoxia-inducible factor α (HIFα).
  • An initial surge in oxidative phosphorylation and reactive oxygen species generation enhances NRF2 activity.
  • NRF2 activation initiates a HIFα-mediated shift towards glycolysis and influences glucose metabolism via the pentose phosphate pathway.
  • Inhibition of NRF2 compromises metabolic reprogramming and significantly reduces iPSC colony formation efficiency.

Conclusions:

  • NRF2 plays a critical role in mediating the metabolic reprogramming essential for efficient iPSC generation.
  • The interplay between oxidative stress, NRF2, and the glycolytic shift is a key determinant of reprogramming success.
  • Targeting NRF2 and associated metabolic pathways may offer strategies to improve iPSC generation efficiency.