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Review
. 2021 Jan 25:25:100905.
doi: 10.1016/j.bbrep.2020.100905. eCollection 2021 Mar.

More attention on glial cells to have better recovery after spinal cord injury

Sajad Hassanzadeh  1   2 , Maryam Jalessi  1 , Seyed Behnamedin Jameie  2   3 , Mehdi Khanmohammadi  1 , Zohre Bagher  4 , Zeinab Namjoo  5 , Seyed Mohammad Davachi  6
Affiliations
Review

More attention on glial cells to have better recovery after spinal cord injury

Sajad Hassanzadeh et al. Biochem Biophys Rep. .

Abstract

Functional improvement after spinal cord injury remains an unsolved difficulty. Glial scars, a major component of SCI lesions, are very effective in improving the rate of this recovery. Such scars are a result of complex interaction mechanisms involving three major cells, namely, astrocytes, oligodendrocytes, and microglia. In recent years, scientists have identified two subtypes of reactive astrocytes, namely, A1 astrocytes that induce the rapid death of neurons and oligodendrocytes, and A2 astrocytes that promote neuronal survival. Moreover, recent studies have suggested that the macrophage polarization state is more of a continuum between M1 and M2 macrophages. M1 macrophages that encourage the inflammation process kill their surrounding cells and inhibit cellular proliferation. In contrast, M2 macrophages promote cell proliferation, tissue growth, and regeneration. Furthermore, the ability of oligodendrocyte precursor cells to differentiate into adult oligodendrocytes or even neurons has been reviewed. Here, we first scrutinize recent findings on glial cell subtypes and their beneficial or detrimental effects after spinal cord injury. Second, we discuss how we may be able to help the functional recovery process after injury.

Keywords: A1 astrocyte; A2 astrocyte; CNS, Central Nervous System; M1 and M2 macrophages; OPCs; OPCs, Oligodendrocytes Progenitor Cells; SCI, Spinal Cord Injury; Spinal cord injury.

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Conflict of interest statement

I wish to confirm that there are no known conflicts of interest associated with this publication and there has been no significant financial support for this work that could have influenced its outcome. I confirm that the manuscript has been read and approved by all named authors and that there are no other persons who satisfied the criteria for authorship but are not listed. I further confirm that the order of authors listed in the manuscript has been approved by all of authors. I confirm that the authors have given due consideration to the protection of intellectual property associated with this work and that there are no impediments to publication, including the timing of publication, with respect to intellectual property. In so doing I confirm that we have followed the regulations of our institutions concerning intellectual property.

Figures

Fig. 1
Fig. 1
Changes in the morphology and function of quiescent astrocytes after an injury to the spinal cord. Quiescent astrocytes are able to be divided into reactive and scar-forming astrocytes; reactive astrocytes can be further classified into A1 and A2 astrocytes. Each of these cells has its own markers and functions after SCI.
Fig. 2
Fig. 2
Activation of Neuro D1 has effects on the microenvironment of injured neural tissue through: 1. generation of new neurons 2. reduction of toxic A1 astrocytes (increase in A2 astrocyte activity) 3. attenuation of toxic M1 microglia, and 4. repair of blood vessels and BBB integrity.
Fig. 3
Fig. 3
The three main sources of Macrophage cells after spinal cord injury (SCI) are represented in numeric format. The first wave of Macrophage influx occurs on day 3 and reaches a peak on day 7. The second wave begins on day 14 and peaks again on day 60. The main source of first wave macrophages is the spleen and mostly contains M1 Macrophage and the second wave of macrophages could be from either the bone marrow or from a self-renewing source at the injury sites and contains both M1 and M2 macrophages.
Fig. 4
Fig. 4
Time-course profiles of microglial activation after SCI.
See this image and copyright information in PMC

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