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      Exosomes and Cardiovascular Protection

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          Abstract

          Most, if not all, cells of the cardiovascular system secrete small, lipid bilayer vesicles called exosomes. Despite technical challenges in their purification and analysis, exosomes from various sources have been shown to be powerfully cardioprotective. Indeed, it is possible that much of the so-called “paracrine” benefit in cardiovascular function obtained by stem cell therapy can be replicated by the injection of exosomes produced by stem cells. However, exosomes purified from plasma appear to be just as capable of activating cardioprotective pathways. We discuss the potential roles of endogenous exosomes in the cardiovascular system, how this is perturbed in cardiovascular disease, and evaluate their potential as therapeutic agents to protect the heart.

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          Biogenesis and secretion of exosomes.

          Joanna Kowal, Mercedes Tkach, Clotilde Théry (2014)
          Although observed for several decades, the release of membrane-enclosed vesicles by cells into their surrounding environment has been the subject of increasing interest in the past few years, which led to the creation, in 2012, of a scientific society dedicated to the subject: the International Society for Extracellular Vesicles. Convincing evidence that vesicles allow exchange of complex information fuelled this rise in interest. But it has also become clear that different types of secreted vesicles co-exist, with different intracellular origins and modes of formation, and thus probably different compositions and functions. Exosomes are one sub-type of secreted vesicles. They form inside eukaryotic cells in multivesicular compartments, and are secreted when these compartments fuse with the plasma membrane. Interestingly, different families of molecules have been shown to allow intracellular formation of exosomes and their subsequent secretion, which suggests that even among exosomes different sub-types exist. Copyright © 2014 Elsevier Ltd. All rights reserved.
          Article 0 comments Cited 796 times – based on 0 reviews     Review now
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            Electron microscopic evidence for externalization of the transferrin receptor in vesicular form in sheep reticulocytes

            K. Teng, M Adam Mahmood, C Wu … (1985)
            Using ferritin-labeled protein A and colloidal gold-labeled anti-rabbit IgG, the fate of the sheep transferrin receptor has been followed microscopically during reticulocyte maturation in vitro. After a few minutes of incubation at 37 degrees C, the receptor is found on the cell surface or in simple vesicles of 100-200 nm, in which the receptor appears to line the limiting membrane of the vesicles. With time (60 min or longer), large multivesicular elements (MVEs) appear whose diameter may reach 1-1.5 micron. Inside these large MVEs are round bodies of approximately 50-nm diam that bear the receptor at their external surfaces. The limiting membrane of the large MVEs is relatively free from receptor. When the large MVEs fuse with the plasma membrane, their contents, the 50-nm bodies, are released into the medium. The 50-nm bodies appear to arise by budding from the limiting membrane of the intracellular vesicles. Removal of surface receptor with pronase does not prevent exocytosis of internalized receptor. It is proposed that the exocytosis of the approximately 50-nm bodies represents the mechanism by which the transferrin receptor is shed during reticulocyte maturation.
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              Endocytosis and intracellular processing of transferrin and colloidal gold-transferrin in rat reticulocytes: demonstration of a pathway for receptor shedding.

              P. Skov, John C S Harding, I Heuser (1984)
              Endocytosis and intracellular processing of transferrin (Tf) and Tf receptors were examined in rat reticulocytes. Subcellular fractionation revealed that Tf enters a non-lysosomal endocytic compartment with a density between those of plasma membrane and lysosomes. After 20 min of uptake at (37 degrees C) 35 to 40% of cell-associated Tf was contained in this intermediate-density compartment. To test the fidelity of colloidal gold-Tf (AuTf) as a probe for Tf processing, reticulocytes were fractionated after uptake of 131I-Tf and 125I-AuTf. The subcellular distributions of the two ligands were indistinguishable by this method, a result suggesting that AuTf is processed similarly to Tf. Electron microscopy revealed that AuTf entered multivesicular endosomes (MVEs) as well as various small vesicles and tubular structures. In addition MVE exocytosis was observed with discharge of inclusion vesicles and associated AuTf. AuTf was bound to the outside of these vesicles both before and after exocytosis. These data suggest that Tf receptors are shed from developing reticulocytes by incorporation into the limiting membrane of inclusion vesicles, followed by discharge of these vesicles by MVE exocytosis. As further evidence of this process, we isolated inclusion vesicles after their discharge and found them to contain Tf receptors. Moreover, the rate of Tf receptor shedding by inclusion vesicle discharge matches Tf receptor loss rates closely enough to suggest that this is the primary path of receptor loss during reticulocyte development.
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                Author and article information

                Contributors
                Sean M. Davidson: +44 203 447 5732 , s.davidson@ucl.ac.uk
                Journal
                Journal ID (nlm-ta): Cardiovasc Drugs Ther
                Journal ID (iso-abbrev): Cardiovasc Drugs Ther
                Title: Cardiovascular Drugs and Therapy
                Publisher: Springer US (New York )
                ISSN (Print): 0920-3206
                ISSN (Electronic): 1573-7241
                Publication date (Electronic): 29 October 2016
                Publication date PMC-release: 29 October 2016
                Publication date (Print): 2017
                Volume: 31
                Issue: 1
                Pages: 77-86
                Affiliations
                The Hatter Cardiovascular Institute, 67 Chenies Mews, WC1E 6HX, London, UK
                Article
                Publisher ID: 6698
                DOI: 10.1007/s10557-016-6698-6
                PMC ID: 5346599
                PubMed ID: 27796607
                SO-VID: 0b131216-3588-45f7-8588-f07b51926cf0
                Copyright © © The Author(s) 2016
                License:

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Funding
                Funded by: British Heart Foundation (GB)
                Funded by: Biomedical Research Council
                Award ID: BRC233/CM/SD/101320
                Award Recipient :
                Funded by: Department of Health’s NIHR Biomedical Research Centres funding scheme
                Categories
                Subject: Original Article
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media New York 2017

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: exosomes,microvesicles,microparticles,stem cells,cardioprotection
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: exosomes, microvesicles, microparticles, stem cells, cardioprotection

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