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Al-Sammarraie et al. Neuroimmunol Neuroinflammation 2021;8:53-63   Neuroimmunology
               DOI: 10.20517/2347-8659.2020.34                              and Neuroinflammation




               Editorial                                                                     Open Access


               Bone morphogenic protein signaling in spinal cord
               injury


               Nadia Al-Sammarraie, Swapan K. Ray

               Department  of  Pathology,  Microbiology,  and  Immunology,  University  of  South  Carolina  School  of  Medicine,  Columbia,  SC
               29209, USA.
               Correspondence to: Prof. Swapan K. Ray, Department of Pathology, Microbiology, and Immunology, University of South Carolina
               School of Medicine, 6439 Garners Ferry Road, Columbia, SC 29209, USA. E-mail: swapan.ray@uscmed.sc.edu
               How to cite this article: Al-Sammarraie N, Ray SK. Bone morphogenic protein signaling in spinal cord injury. Neuroimmunol
               Neuroinflammation 2021;8:53-63. http://dx.doi.org/10.20517/2347-8659.2020.34

               Received: 24 Apr 2020    Accepted: 30 Apr 2020     Fisrt online: 4 Sep 2020     Published: 21 Mar 2021
               Science Editor: Gang Zhao    Copy Editor: Jing-Wen Zhang    Production Editor: Tian Zhang


               Abstract
               Spinal cord injury (SCI) is a debilitating injury that results from traumatic or non-traumatic insults to the spinal
               cord, causing significant impairment of the patient’s activity and quality of life. Bone morphogenic proteins
               (BMPs) are a group of polyfunctional cytokines belonging to the transforming growth factor beta superfamily
               that regulates a wide variety of cellular functions in healthy and disease states. Recent studies suggest that
               dysregulation of BMP signaling is involved in neuronal demyelination and death after traumatic SCI. The focus
               of this article is to describe our current understanding of the role of BMP signaling in the regulation of cell fate,
               proliferation, apoptosis, autophagy, and inflammation in traumatic SCI. First, we will describe the expression of
               BMPs and pattern of BMP signaling before and after traumatic SCI in rodent models and in vitro. Next, we will
               discuss the role of BMP in the regulation of neuronal and glial cell differentiation, survival, functional recovery from
               traumatic SCI, and the gap in knowledge in this area that requires further investigation to improve SCI prognosis.

               Keywords: Spinal cord injury, bone morphogenic protein, apoptosis, proliferation, autophagy, differentiation,
               inflammation



               INTRODUCTION
               Spinal cord injury (SCI) can be either traumatic or non-traumatic damage to the spinal cord and has a
                                                                                            [1-3]
               peak prevalence of approximately 906-1800 cases per million people in the United States . SCI usually
                                                                                               [4]
               causes complete or partial motor and sensory neurological deficits with deleterious outcomes . Traumatic
               SCI can be caused by major trauma to the spinal cord following road traffic accidents, falls in the elderly,
                                                [1,3]
               and violent and sport-related injuries . Non-traumatic SCI usually result from ischemic-reperfusion
                           © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as 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.


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