Glial-Neuronal Interactions in Pathogenesis and Treatment of Spinal Cord Injury
Traumatic spinal cord injury (SCI) elicits an acute inflammatory response which comprises numerous cell populations. It is driven by the immediate response of macrophages and microglia, which triggers activation of genes responsible for the dysregulated microenvironment within the lesion site and in...
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Published in | International journal of molecular sciences Vol. 22; no. 24; p. 13577 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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17.12.2021
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Abstract | Traumatic spinal cord injury (SCI) elicits an acute inflammatory response which comprises numerous cell populations. It is driven by the immediate response of macrophages and microglia, which triggers activation of genes responsible for the dysregulated microenvironment within the lesion site and in the spinal cord parenchyma immediately adjacent to the lesion. Recently published data indicate that microglia induces astrocyte activation and determines the fate of astrocytes. Conversely, astrocytes have the potency to trigger microglial activation and control their cellular functions. Here we review current information about the release of diverse signaling molecules (pro-inflammatory vs. anti-inflammatory) in individual cell phenotypes (microglia, astrocytes, blood inflammatory cells) in acute and subacute SCI stages, and how they contribute to delayed neuronal death in the surrounding spinal cord tissue which is spared and functional but reactive. In addition, temporal correlation in progressive degeneration of neurons and astrocytes and their functional interactions after SCI are discussed. Finally, the review highlights the time-dependent transformation of reactive microglia and astrocytes into their neuroprotective phenotypes (M2a, M2c and A2) which are crucial for spontaneous post-SCI locomotor recovery. We also provide suggestions on how to modulate the inflammation and discuss key therapeutic approaches leading to better functional outcome after SCI. |
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AbstractList | Traumatic spinal cord injury (SCI) elicits an acute inflammatory response which comprises numerous cell populations. It is driven by the immediate response of macrophages and microglia, which triggers activation of genes responsible for the dysregulated microenvironment within the lesion site and in the spinal cord parenchyma immediately adjacent to the lesion. Recently published data indicate that microglia induces astrocyte activation and determines the fate of astrocytes. Conversely, astrocytes have the potency to trigger microglial activation and control their cellular functions. Here we review current information about the release of diverse signaling molecules (pro-inflammatory vs. anti-inflammatory) in individual cell phenotypes (microglia, astrocytes, blood inflammatory cells) in acute and subacute SCI stages, and how they contribute to delayed neuronal death in the surrounding spinal cord tissue which is spared and functional but reactive. In addition, temporal correlation in progressive degeneration of neurons and astrocytes and their functional interactions after SCI are discussed. Finally, the review highlights the time-dependent transformation of reactive microglia and astrocytes into their neuroprotective phenotypes (M2a, M2c and A2) which are crucial for spontaneous post-SCI locomotor recovery. We also provide suggestions on how to modulate the inflammation and discuss key therapeutic approaches leading to better functional outcome after SCI. |
Author | Lukacova, Nadezda Galik, Jan Bacova, Maria Kisucka, Alexandra Kuruc, Tomas Ileninova, Maria Kiss Bimbova, Katarina |
AuthorAffiliation | Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4–6, 040 01 Kosice, Slovakia; kisucka@saske.sk (A.K.); bimbova@saske.sk (K.K.B.); bacova@saske.sk (M.B.); ileninova@saske.sk (M.I.); kuruc@saske.sk (T.K.); galik@saske.sk (J.G.) |
AuthorAffiliation_xml | – name: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4–6, 040 01 Kosice, Slovakia; kisucka@saske.sk (A.K.); bimbova@saske.sk (K.K.B.); bacova@saske.sk (M.B.); ileninova@saske.sk (M.I.); kuruc@saske.sk (T.K.); galik@saske.sk (J.G.) |
Author_xml | – sequence: 1 givenname: Nadezda surname: Lukacova fullname: Lukacova, Nadezda organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia – sequence: 2 givenname: Alexandra surname: Kisucka fullname: Kisucka, Alexandra organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia – sequence: 3 givenname: Katarina orcidid: 0000-0001-9920-3665 surname: Kiss Bimbova fullname: Kiss Bimbova, Katarina organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia – sequence: 4 givenname: Maria surname: Bacova fullname: Bacova, Maria organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia – sequence: 5 givenname: Maria surname: Ileninova fullname: Ileninova, Maria organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia – sequence: 6 givenname: Tomas orcidid: 0000-0002-0890-9548 surname: Kuruc fullname: Kuruc, Tomas organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia – sequence: 7 givenname: Jan surname: Galik fullname: Galik, Jan organization: Institute of Neurobiology, Biomedical Research Centre, Slovak Academy of Sciences, Soltesovej 4-6, 040 01 Kosice, Slovakia |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34948371$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | 2021 by the authors. 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 (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2021 by the authors. 2021 |
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Keywords | lesion microenvironment rehabilitation intercellular crosstalk neuroinflammation electrostimulation in vivo glia-to neuron reprogramming neuroprotective strategies subpial delivery microglia and astrocytes phenotypes gut dysbiosis |
Language | English |
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Snippet | Traumatic spinal cord injury (SCI) elicits an acute inflammatory response which comprises numerous cell populations. It is driven by the immediate response of... |
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SubjectTerms | Animals Apoptosis Astrocytes Chemokines Contusions Cytokines Degeneration Disease Management Gene expression Homeostasis Humans in vivo glia-to neuron reprogramming Inflammation Inflammation - metabolism Inflammation - pathology Inflammation - therapy Inflammatory response intercellular crosstalk lesion microenvironment Ligands Macrophages Microenvironments Microglia microglia and astrocytes phenotypes Neurogenesis Neuroglia - metabolism Neuroglia - pathology neuroinflammation Neuronal-glial interactions Neurons - metabolism Neurons - pathology Neuroprotection Neurotoxicity Neutrophils Nitric oxide Parenchyma Pathogenesis Phenotypes Review Spinal Cord - metabolism Spinal Cord - pathology Spinal cord injuries Spinal Cord Injuries - metabolism Spinal Cord Injuries - pathology Spinal Cord Injuries - therapy subpial delivery Transcription activation Trauma Tumor necrosis factor-TNF |
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Title | Glial-Neuronal Interactions in Pathogenesis and Treatment of Spinal Cord Injury |
URI | https://www.ncbi.nlm.nih.gov/pubmed/34948371 https://www.proquest.com/docview/2612803540/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC8708227 https://doaj.org/article/d87da0f6829d485cba3fb4ca48f0bc96 |
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