How Transplanted Stem Cells Behave in Injured Spinal Cord Tissue

A representative confocal image of spinal cord tissue fluorescently immunolabeled for SC121 in conjunction with GFAP – markers that allowed the researchers to track stem cell differentiation and migration by stereological quantification. (Image provided by study author Dr. Aileen J. Anderson)

A representative confocal image of spinal cord tissue fluorescently immunolabeled for SC121 (red) in conjunction with GFAP (green) – markers that allowed researchers to quantify stem cell differentiation and migration. (Image provided by study author Dr. Aileen J. Anderson)

Research has shown that transplanting human neural stem cells into damaged spinal cords restores locomotor function in a mouse model of spinal cord injury1. Researchers who worked on that study have published another paper examining how these neural stem cells behave in injured tissue as they aid in healing. Learning how stem cells behave in injured tissue will hopefully help researchers develop better treatments for spinal cord injuries.

In the study, researchers used Stereo Investigator to stereologically quantify the survival, migration, proliferation, and differentiation of human neural stem cells transplanted into injured and uninjured mice. Stem cells were analyzed in mouse brain tissue specimens 1, 7, 14, 28, and 98 days after transplantation. The research found that there were fewer stem cells in the injured animals compared to the uninjured animals at all time points, stem cells in injured mice localized near the center of the injury, a delay of stem cell proliferation in injured tissue led to an overall deficit of actively dividing cells, proliferation in injured mice occurred closer to the injection sites (the locations where the stem cells were injected into the mice), and the injured microenvironment increased differentiation to more mature oligodendrocytes.

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Scientists Use Stereo Investigator in Spinal Cord Injury Study

Stereo Investigator Graphic

After an initial spinal cord injury, a cascading series of secondary events continues to do damage to the nervous system. One particularly damaging event is the death of oligodendrocytes—neuroglial cells that help protect and support the central nervous system. Scientists are learning more about the mechanisms involved in this process in the hope that their research may lead to the development of new therapeutic treatments for stopping some of the secondary damage before it occurs.

Researchers at the Miami Project to Cure Paralysis previously found that astrocytes play a role in oligodendrocyte death after spinal cord injury, but they weren’t quite sure how. Their new study identifies a culprit – an enzyme called NADPH oxidase. According to their paper, published in PLOS One, astrocytes activate NADPH oxidase within oligodendrocytes after an injury, triggering a toxic effect in the tiny neural cells.

In their study, the researchers set out to see what would happen if they could prevent post-trauma NADPH oxidase activation. Their results proved promising, with both in vitro and in vivo experiments resulting in lower oligodendrocyte death.

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Stereo Investigator Contributes to Study Showing Low Zinc Levels Associated With More Cell Deaths in Spinal Cord Injury

iStock_spinal_cord_xray

Spinal cord injuries can result in a range of physical disabilities from slight loss of motor function to major paralysis, but little is known about the mechanisms underlying the damage. Scientists affiliated with the Miami Project to Cure Paralysis at the University of Miami are gaining knowledge about how the nervous system responds to spinal cord injuries. Their latest study, published last month in the Journal of Neuroscience Research, suggests that post trauma cell death is associated with low zinc levels.

“The expression of functional NF-kB signaling resulted in a reduction in extracellular zinc levels, thereby inducing glutamate-induced cell death,” the authors say in their paper “Reduced Extracellular Zinc Levels Facilitate Glutamate-Mediated Oligodendrocyte Death After Trauma.

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