Abstract
Stem cell therapies are currently gaining momentum in the treatment of spinal cord injury (SCI). However, unsatisfied intrinsic neurite growth capacity constitutes significant obstacles for injured spinal cord repair and ultimately results in neurological dysfunction. The present study assessed the efficacy of thrombospondin-1 (TSP-1), a neurite outgrowth-promoting molecule, modified bone marrow mesenchymal stem cells (BMSCs) on promoting neurite outgrowth in vitro and in vivo of Oxygen–Glucose Deprivation (OGD) treated motor neurons and SCI rat models. The present results demonstrated that the treatment of BMSCs+TSP-1 could promote the neurite length, neuronal survival, and functional recovery after SCI. Additionally, TSP-1 could activate transforming growth factor-β1 (TGF-β1) then induced the smad2 phosphorylation, and expedited the expression of GAP-43 to promote neurite outgrowth. The present study for the first time demonstrated that BMSCs+TSP-1 could promote neurite outgrowth and functional recovery after SCI partly through the TGF-β1/p-Samd2 pathway. The study provided a novel encouraging evidence for the potential treatment of BMSCs modification with TSP-1 in patients with SCI.
Highlights
Spinal cord injury (SCI) becomes a major public health issue that impairs motor, sensory, autonomic function, and results in neurological dysfunctions in patients with spinal cord injury (SCI) [1, 2]
The present results demonstrated that the treatment of bone marrow mesenchymal stem cells (BMSCs)+TSP-1 could promote the neurite length, neuronal survival, and functional recovery after SCI
The results demonstrated that the ratio of phosphorylation of Smad2 was significantly increased in the SCI+BMSCS+TSP-1 group when compared with the SCI+vehicle group, SCI+BMSCS group and SCI+BMSCS-TSP-1 group after 3 days (Figure 8D, 8G, P
Summary
Spinal cord injury (SCI) becomes a major public health issue that impairs motor, sensory, autonomic function, and results in neurological dysfunctions in patients with SCI [1, 2]. The pathology of SCI can be classified into primary and secondary injury. Primary injury often results from mechanical impaction to the spine. Secondary injury refers to the multifaceted pathological mechanisms that start after primary SCI and include a breakdown of bloodspinal cord barrier (BSCB), neuroinflammation, oxidative stress and neuronal apoptosis [4,5,6]. The pathology of secondary injury resulting from neural tissue destruction, poor microenvironment, and unsatisfied intrinsic neurite growth capacity can be at least as responsible for longterm dysfunction [7]
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