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.
Highlights
Spinal cord injury (SCI) can be either traumatic or non-traumatic damage to the spinal cord and has a peak prevalence of approximately 906-1800 cases per million people in the United States[1,2,3]
This study found that BMP2, 4, and 7 were expressed in intact spinal cord and their expression was further increased after SCI in the following cell types: neurons, neuronal stem cells (NSCs), microglia, and oligodendrocytes, but not in astrocytes[37]
Bone morphogenic proteins (BMPs) ligands, receptors, and canonical and non-canonical pathways are upregulated after SCI
Summary
Spinal cord injury (SCI) can be either traumatic or non-traumatic damage to the spinal cord and has a peak prevalence of approximately 906-1800 cases per million people in the United States[1,2,3]. Transplanting the above-modified NPCs into a mice model of SCI resulted in improvement of the motor scores with inhibition of astrocytic differentiation and promotion of neuronal and oligodendrocytic differentiations in vivo[38] Together, these studies imply that targeting BMP signaling could be beneficial for ameliorating astrocytic scar formation, and for enhancing oligodendrocytic differentiation for remyelination after SCI. North et al.[39] showed that the conditional deletion of β1 integrin from ependymal stem cells resulted in an increase in their differentiation into astrocytes, which could promote glial scar formation after SCI and reduce BBB motor scores in SCI mice, which were found to be associated with increases in canonical (Smad1/5/8) and non-canonical (p38) signaling. These results suggest different roles of different BMP ligands on neuronal and glial cell survival post-SCI, which requires further investigation
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