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      Mitochondria in the maintenance of hematopoietic stem cells: new perspectives and opportunities

      Author(s): 1 , 2 , 3 , 4 , 5
      Publication date Created:
      Publication date (Print):
      Journal: Blood
      Publisher: American Society of Hematology

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          Abstract

          The hematopoietic system produces new blood cells throughout life. Mature blood cells all derived from a pool of rare long-lived hematopoietic stem cells (HSCs) that are mostly quiescent but occasionally divide and self-renew to maintain the stem cell pool and to insure the continuous replenishment of blood cells. Mitochondria have recently emerged as critical not only for HSC differentiation and commitment but also for HSC homeostasis. Mitochondria are dynamic organelles that orchestrate a number of fundamental metabolic and signaling processes, producing most of the cellular energy via oxidative phosphorylation. HSCs have a relatively high amount of mitochondria that are mostly inactive. Here, we review recent advances in our understanding of the role of mitochondria in HSC homeostasis and discuss, among other topics, how mitochondrial dynamism and quality control might be implicated in HSC fate, self-renewal, and regenerative potential.

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          mTOR controls mitochondrial oxidative function through a YY1-PGC-1alpha transcriptional complex.

          John T Cunningham, Joseph Rodgers, Daniel Arlow … (2007)
          Transcriptional complexes that contain peroxisome-proliferator-activated receptor coactivator (PGC)-1alpha control mitochondrial oxidative function to maintain energy homeostasis in response to nutrient and hormonal signals. An important component in the energy and nutrient pathways is mammalian target of rapamycin (mTOR), a kinase that regulates cell growth, size and survival. However, it is unknown whether and how mTOR controls mitochondrial oxidative activities. Here we show that mTOR is necessary for the maintenance of mitochondrial oxidative function. In skeletal muscle tissues and cells, the mTOR inhibitor rapamycin decreased the gene expression of the mitochondrial transcriptional regulators PGC-1alpha, oestrogen-related receptor alpha and nuclear respiratory factors, resulting in a decrease in mitochondrial gene expression and oxygen consumption. Using computational genomics, we identified the transcription factor yin-yang 1 (YY1) as a common target of mTOR and PGC-1alpha. Knockdown of YY1 caused a significant decrease in mitochondrial gene expression and in respiration, and YY1 was required for rapamycin-dependent repression of those genes. Moreover, mTOR and raptor interacted with YY1, and inhibition of mTOR resulted in a failure of YY1 to interact with and be coactivated by PGC-1alpha. We have therefore identified a mechanism by which a nutrient sensor (mTOR) balances energy metabolism by means of the transcriptional control of mitochondrial oxidative function. These results have important implications for our understanding of how these pathways might be altered in metabolic diseases and cancer.
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            Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization.

            Ann Cassidy-Stone, Jerry E Chipuk, Elena Ingerman … (2008)
            Mitochondrial fusion and division play important roles in the regulation of apoptosis. Mitochondrial fusion proteins attenuate apoptosis by inhibiting release of cytochrome c from mitochondria, in part by controlling cristae structures. Mitochondrial division promotes apoptosis by an unknown mechanism. We addressed how division proteins regulate apoptosis using inhibitors of mitochondrial division identified in a chemical screen. The most efficacious inhibitor, mdivi-1 (for mitochondrial division inhibitor) attenuates mitochondrial division in yeast and mammalian cells by selectively inhibiting the mitochondrial division dynamin. In cells, mdivi-1 retards apoptosis by inhibiting mitochondrial outer membrane permeabilization. In vitro, mdivi-1 potently blocks Bid-activated Bax/Bak-dependent cytochrome c release from mitochondria. These data indicate the mitochondrial division dynamin directly regulates mitochondrial outer membrane permeabilization independent of Drp1-mediated division. Our findings raise the interesting possibility that mdivi-1 represents a class of therapeutics for stroke, myocardial infarction, and neurodegenerative diseases.
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              Mitochondrial dynamics and inheritance during cell division, development and disease.

              Prashant Mishra, David Chan (2014)
              During cell division, it is critical to properly partition functional sets of organelles to each daughter cell. The partitioning of mitochondria shares some common features with that of other organelles, particularly in the use of interactions with cytoskeletal elements to facilitate delivery to the daughter cells. However, mitochondria have unique features - including their own genome and a maternal mode of germline transmission - that place additional demands on this process. Consequently, mechanisms have evolved to regulate mitochondrial segregation during cell division, oogenesis, fertilization and tissue development, as well as to ensure the integrity of these organelles and their DNA, including fusion-fission dynamics, organelle transport, mitophagy and genetic selection of functional genomes. Defects in these processes can lead to cell and tissue pathologies.
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                Author and article information

                Journal
                Title: Blood
                Publisher: American Society of Hematology
                ISSN (Print): 0006-4971
                ISSN (Electronic): 1528-0020
                Publication date Created: May 02 2019
                Publication date (Print): May 02 2019
                Volume: 133
                Issue: 18
                Pages: 1943-1952
                Affiliations
                [1 ]Division of Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital, Cincinnati, OH; and
                [2 ]Department of Cell, Developmental and Regenerative Biology,
                [3 ]Developmental and Stem Cell Biology Multidisciplinary Training, Graduate School of Biomedical Sciences,
                [4 ]Black Family Stem Cell Institute, and
                [5 ]Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY
                Article
                DOI: 10.1182/blood-2018-10-808873
                PMC ID: 6497515
                PubMed ID: 30808633
                SO-VID: 53f7bfad-9b11-43a7-ae2a-c811c6816293
                Copyright © © 2019
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