Mitochondrial plasticity in cell fate regulation
Amir Bahat,Atan Gross +1 more
TLDR
This review focuses on recent findings demonstrating that mitochondria are essential regulators of stem cell activation and fate decisions, and discusses the suggested mechanisms and alternative routes for mitochondria-to-nucleus communications.About:
This article is published in Journal of Biological Chemistry.The article was published on 2019-09-20 and is currently open access. It has received 86 citations till now. The article focuses on the topics: Stem cell & Mitochondrion.read more
Citations
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Journal ArticleDOI
The cell biology of mitochondrial membrane dynamics
TL;DR: How bioenergetics and cellular signalling are linked to dynamic changes of mitochondrial morphology is described, with morphological changes to mitochondria accompanying a multitude of processes as diverse as cell pluripotency, division, differentiation, senescence and death.
Methionine metabolism regulates maintenance and differentiation of human pluripotent stem cells
TL;DR: It is shown that human ESCs/iPSCs require high amounts of methionine (Met) and express high levels of enzymes involved in Met metabolism, and SAM is a key regulator for maintaining undifferentiated pluripotent stem cells and regulating their differentiation.
Journal ArticleDOI
Mitochondrial dynamics in postmitotic cells regulate neurogenesis
TL;DR: Shortly after cortical stem cells have divided, daughter cells destined to self-renew undergo mitochondrial fusion, whereas those that retain high levels of mitochondria fission become neurons, revealing a postmitotic period of fate plasticity in which mitochondrial dynamics are linked with cell fate.
Journal ArticleDOI
Mitochondria as Signaling Organelles Control Mammalian Stem Cell Fate.
TL;DR: In this article, the authors focus on key conceptual ideas on how mitochondria control mammalian stem cell fate and function through reactive oxygen species (ROS) generation, TCA cycle metabolite production, NAD+/NADH ratio regulation, pyruvate metabolism, and mitochondrial dynamics.
Journal ArticleDOI
Platelets facilitate the wound-healing capability of mesenchymal stem cells by mitochondrial transfer and metabolic reprogramming
Jennyfer Levoux,Alexandre Prola,Alexandre Prola,Peggy Lafuste,Marianne Gervais,Nathalie Chevallier,Zeynab Koumaiha,Kaouthar Kefi,Laura Braud,Alain Schmitt,Azzedine Yacia,Aurélie Schirmann,Barbara Hersant,Mounia Sid-Ahmed,Sabrina Ben Larbi,Katerina Komrskova,Katerina Komrskova,Jakub Rohlena,Frédéric Relaix,Frédéric Relaix,Jiri Neuzil,Jiri Neuzil,Anne-Marie Rodriguez +22 more
TL;DR: In this article, the authors demonstrate that platelet-derived mitochondria promote the pro-angiogenic activity of mesenchymal stem cells via their metabolic remodeling, and that activation of the de novo fatty acid synthesis pathway is required for increased secretion of proangiogenesis factors by platelet pre-conditioned MSCs.
References
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Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
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ROS Function in Redox Signaling and Oxidative Stress
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Stem Cells and Niches: Mechanisms That Promote Stem Cell Maintenance throughout Life
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ATP-Citrate Lyase Links Cellular Metabolism to Histone Acetylation
Kathryn E. Wellen,Georgia Hatzivassiliou,Uma M. Sachdeva,Thi Bui,Justin R. Cross,Craig B. Thompson +5 more
TL;DR: It is found that ACL is required for increases in histone acetylation in response to growth factor stimulation and during differentiation, and that glucose availability can affect hist one acetylations in an ACL-dependent manner.
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Mitochondrial transcription factor A is necessary for mtDNA maintenance and embryogenesis in mice
Nils-Göran Larsson,Jianming Wang,Hans Wilhelmsson,Anders Oldfors,Pierre Rustin,Mark Lewandoski,Gregory S. Barsh,David A. Clayton +7 more
TL;DR: The mouse gene for mitochondrial transcription factor A (Tfam), formerly known as m-mtTFA, is disrupted by gene targetting of loxP-sites followed by cre-mediated excision in vivo and is the first mammalian protein demonstrated to regulate mtDNA copy number in vivo.
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