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      Mesenchymal Stem Cells for Spinal Cord Injury: Current Options, Limitations, and Future of Cell Therapy

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          Abstract

          Spinal cord injury (SCI) constitutes an inestimable public health issue. The most crucial phase in the pathophysiological process of SCI concerns the well-known secondary injury, which is the uncontrolled and destructive cascade occurring later with aberrant molecular signaling, inflammation, vascular changes, and secondary cellular dysfunctions. The use of mesenchymal stem cells (MSCs) represents one of the most important and promising tested strategies. Their appeal, among the other sources and types of stem cells, increased because of their ease of isolation/preservation and their properties. Nevertheless, encouraging promise from preclinical studies was followed by weak and conflicting results in clinical trials. In this review, the therapeutic role of MSCs is discussed, together with their properties, application, limitations, and future perspectives.

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          Paracrine mechanisms of mesenchymal stem cell-based therapy: current status and perspectives.

          Xiaoting Liang, Yue Ding, Yuelin Zhang … (2014)
          Mesenchymal stem cells (MSCs) are one of a few stem cell types to be applied in clinical practice as therapeutic agents for immunomodulation and ischemic tissue repair. In addition to their multipotent differentiation potential, a strong paracrine capacity has been proposed as the principal mechanism that contributes to tissue repair. Apart from cytokine/chemokine secretion, MSCs also display a strong capacity for mitochondrial transfer and microvesicle (exosomes) secretion in response to injury with subsequent promotion of tissue regeneration. These unique properties of MSCs make them an invaluable cell type to repair damaged tissues/organs. Although MSCs offer great promise in the treatment of degenerative diseases and inflammatory disorders, there are still many challenges to overcome prior to their widespread clinical application. Particularly, their in-depth paracrine mechanisms remain a matter for debate and exploration. This review will highlight the discovery of the paracrine mechanism of MSCs, regulation of the paracrine biology of MSCs, important paracrine factors of MSCs in modulation of tissue repair, exosome and mitochondrial transfer for tissue repair, and the future perspective for MSC-based therapy.
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            The Biology of Regeneration Failure and Success After Spinal Cord Injury.

            Amanda Phuong Tran, Philippa Mary Warren, Jerry Silver (2018)
            Since no approved therapies to restore mobility and sensation following spinal cord injury (SCI) currently exist, a better understanding of the cellular and molecular mechanisms following SCI that compromise regeneration or neuroplasticity is needed to develop new strategies to promote axonal regrowth and restore function. Physical trauma to the spinal cord results in vascular disruption that, in turn, causes blood-spinal cord barrier rupture leading to hemorrhage and ischemia, followed by rampant local cell death. As subsequent edema and inflammation occur, neuronal and glial necrosis and apoptosis spread well beyond the initial site of impact, ultimately resolving into a cavity surrounded by glial/fibrotic scarring. The glial scar, which stabilizes the spread of secondary injury, also acts as a chronic, physical, and chemo-entrapping barrier that prevents axonal regeneration. Understanding the formative events in glial scarring helps guide strategies towards the development of potential therapies to enhance axon regeneration and functional recovery at both acute and chronic stages following SCI. This review will also discuss the perineuronal net and how chondroitin sulfate proteoglycans (CSPGs) deposited in both the glial scar and net impede axonal outgrowth at the level of the growth cone. We will end the review with a summary of current CSPG-targeting strategies that help to foster axonal regeneration, neuroplasticity/sprouting, and functional recovery following SCI.
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              G-CSF induces stem cell mobilization by decreasing bone marrow SDF-1 and up-regulating CXCR4.

              Isabelle Petit, Martine Szyper-Kravitz, Arnon Nagler … (2002)
              Granulocyte colony-stimulating factor (G-CSF) induced hematopoietic stem cell mobilization is widely used for clinical transplantation; however, the mechanism is poorly understood. We report here that G-CSF induced a reduction of the chemokine stromal cell derived factor 1 (SDF-1) and an increase in its receptor CXCR4 in the bone marrow (BM), whereas their protein expression in the blood was less affected. The gradual decrease of BM SDF-1, due mostly to its degradation by neutrophil elastase, correlated with stem cell mobilization. Elastase inhibition reduced both activities. Human and murine stem cell mobilization was inhibited by neutralizing CXCR4 or SDF-1 antibodies, demonstrating SDF-1 CXCR4 signaling in cell egress. We suggest that manipulation of SDF-1 CXCR4 interactions may be a means with which to control the navigation of progenitors between the BM and blood to improve the outcome of clinical stem cell transplantation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 31 May 2019
                Publication date Collection: June 2019
                Volume: 20
                Issue: 11
                Electronic Location Identifier: 2698
                Affiliations
                [1 ]Department of Neuroscience “Rita Levi Montalcini”, Neurosurgery Unit, University of Turin, 10126 Turin, Italy; mmonticelli89@ 123456gmail.com (M.M.); zenga.francesco@ 123456gmail.com (F.Z.); aducati.nch@ 123456gmail.com (A.D.); dgarbossa@ 123456gmail.com (D.G.)
                [2 ]Department of Neuroscience “Rita Levi Montalcini”, Neuroscience Institute “Cavalieri Ottolenghi”, University of Turin, Consorzio Istituto Nazionale di Neuroscienze, 10043 Orbassano, Italy; marina.boido@ 123456unito.it (M.B.); alessandro.vercelli@ 123456unito.it (A.V.)
                Author notes
                [* ]Correspondence: fabio.cofano@ 123456unito.it
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-1211-1552
                Article
                Publisher ID: ijms-20-02698
                DOI: 10.3390/ijms20112698
                PMC ID: 6600381
                PubMed ID: 31159345
                SO-VID: 3b814cf3-3087-4ae2-a78b-bdd5f34e7410
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 17 April 2019
                Date accepted : 30 May 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: mesenchymal stem cells,spinal cord injury,regenerative medicine,translational medicine
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: mesenchymal stem cells, spinal cord injury, regenerative medicine, translational medicine

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