Abstract
Human mesenchymal stem cells derived from Wharton’s jelly (WJ-MSCs) were used for the treatment of the ischemic-compression model of spinal cord injury in rats. To assess the effectivity of the treatment, different dosages (0.5 or 1.5 million cells) and repeated applications were compared. Cells or saline were applied intrathecally by lumbar puncture for one week only, or in three consecutive weeks after injury. Rats were assessed for locomotor skills (BBB, rotarod, flat beam) for 9 weeks. Spinal cord tissue was morphometrically analyzed for axonal sprouting, sparing of gray and white matter and astrogliosis. Endogenous gene expression (Gfap, Casp3, Irf5, Cd86, Mrc1, Cd163) was studied with quantitative Real-time polymerase chain reaction (qRT PCR). Significant recovery of functional outcome was observed in all of the treated groups except for the single application of the lowest number of cells. Histochemical analyses revealed a gradually increasing effect of grafted cells, resulting in a significant increase in the number of GAP43+ fibers, a higher amount of spared gray matter and reduced astrogliosis. mRNA expression of macrophage markers and apoptosis was downregulated after the repeated application of 1.5 million cells. We conclude that the effect of hWJ-MSCs on spinal cord regeneration is dose-dependent and potentiated by repeated application.
Highlights
Spinal cord injury (SCI) is a serious mutilating injury, resulting in loss of motor, sensory, and autonomic functions, and remains a challenging medical and social problem even in the 21st century
Since there is no specific treatment for primary injury, and the endogenous potential to regenerate the spinal cord neurons is very limited [2], several treatments are focused on neuroprotection and/or reducing the impact of secondary pathological processes
Recovery of the hind limb locomotor function was evaluated every week starting the first week after SCI
Summary
Spinal cord injury (SCI) is a serious mutilating injury, resulting in loss of motor, sensory, and autonomic functions, and remains a challenging medical and social problem even in the 21st century. The final neurological deficit is determined by two mechanisms—primary and secondary injury. Primary injury represents the mechanism and strength of the direct trauma. Secondary injury is characterized by the local immune reaction followed by apoptosis of the injured and vulnerable neurons, tissue atrophy with cavitation, and glial scar formation [1]. Since there is no specific treatment for primary injury, and the endogenous potential to regenerate the spinal cord neurons is very limited [2], several treatments are focused on neuroprotection and/or reducing the impact of secondary pathological processes. Promising results in alleviation of the pathological chain of secondary damage were found in the last decade by application of mesenchymal stem cells (MSCs)
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