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Review
. 2017 Dec;20(12):1287-1296.
doi: 10.22038/IJBMS.2017.9620.

Mechanisms of spinal cord injury regeneration in zebrafish: a systematic review

Zeynab Noorimotlagh  1 , Mahla Babaie  1 , Mahdi Safdarian  2 , Tahereh Ghadiri  3 , Vafa Rahimi-Movaghar  4
Affiliations
Review

Mechanisms of spinal cord injury regeneration in zebrafish: a systematic review

Zeynab Noorimotlagh et al. Iran J Basic Med Sci. 2017 Dec.

Abstract

Objectives: To determine the molecular and cellular mechanisms of spinal cord regeneration in zebrafish.

Materials and methods: Medical databases of PubMed and Scopus were searched with following key words: Zebrafish; spinal cord injuries; regeneration; recovery of function. The map of mechanisms was performed using Xmind software.

Results: Wnt/ß-catenin signaling, L1.1, L1.2, Major vault protein (MVP), contactin-2 and High mobility group box1 (HMGB1) had positive promoting effects on axonal re-growth while Ptena had an inhibitory effect. Neurogenesis is stimulated by Wnt/ß-catenin signaling as well as HMGB1, but inhibited by Notch signaling. Glial cells proliferate in response to fibroblast growth factor (FGF) signaling and Lysophosphatidic acid (LPA). Furthermore, fgf signaling pathway causes glia bridge formation in favor of axonal regeneration. LPA and HMGB1 in acute phase stimulate inflammatory responses around injury and suppress regeneration. LPA also induces microglia activation and neuronal death in addition to glia cell proliferation, but prevents neurite sprouting.

Conclusion: This study provides a comprehensive review of the known molecules and mechanisms in the current literature involved in the spinal cord injury (SCI) regeneration in zebrafish, in a time course manner. A better understanding of the whole determining mechanisms for the SCI regeneration should be considered as a main goal for future studies.

Keywords: Regeneration recovery-of function; Spinal cord injuries; Spinal cord regeneration; Zebrafish.

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Figures

Figure 1
Figure 1
Time course concept map
Figure 2
Figure 2
Cellular concept map
See this image and copyright information in PMC

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References

    1. Pinto L, Gotz M. Radial glial cell heterogeneity-the source of diverse progeny in the CNS. Prog Neurobiol. 2007;83:2–23. - PubMed
    1. Rahimi-Movaghar V, Yazdi A, Karimi M, Mohammadi M, Firouzi M, Zanjani LO, et al. Effect of decompression on complete spinal cord injury in rats. International J Neurosci. 2008;118:1359–1373. - PubMed
    1. Rahimi-Movaghar V, Vaccaro AR, Mohammadi M. Efficacy of surgical decompression in regard to motor recovery in the setting of conus medullaris injury. J Spinal Cord Med. 2006;29:32–38. - PMC - PubMed
    1. Rahimi-Movaghar V, Saadat S, Vaccaro AR, Ghodsi SM, Samadian M, Sheykhmozaffari A, et al. The efficacy of surgical decompression before 24 hours versus 24 to 72 hours in patients with spinal cord injury from T1 to L1–with specific consideration on ethics: a randomized controlled trial. Trials. 2009;10:77. - PMC - PubMed
    1. Rahimi-Movaghar V, Sayyah MK, Akbari H, Khorramirouz R, Rasouli MR, Moradi-Lakeh M, et al. Epidemiology of traumatic spinal cord injury in developing countries: a systematic review. Neuroepidemiology. 2013;41:65–85. - PubMed

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