Bone Marrow Derived Stem Cells Investigated For Stroke Therapy
Stem cell researchers in Japan investigating bone marrow stromal cells may have discovered how to restore lost neurologic function when transplanted into animals exhibiting central nervous system disorders.
"Our study showed that cell transplantation therapy may improve brain receptor function in patients who suffered from cerebral stroke, improving their neurological symptoms," said Satoshi Kuroda, M.D., Ph.D., who is with the department of neurosurgery at Hokkaido University School of Medicine in Sapporo, Japan. "How the transplanted bone marrow stromal cells restore the lost neurologic function is not clear," added the co-author of "Improved Expression of a-Aminobutyric Acid Receptor in Mice With Cerebral Infarct and Transplanted Bone Marrow Stromal Cells: An Autoradiographic and Histologic Analysis."
Thus far, researchers hope that that cells found in an adult’s bone marrow (stromal stem cells) may provide a safe source for replacing brain cells lost to neurological diseases like Alzheimer’s and Parkinson’s.
Studies around the world has indicated that stem cells taken from adult human bone marrow may differentiate into neural cells that could then possibly be transplanted into the brain.
This study's findings demonstrated that bone marrow stromal cells "may contribute to neural tissue regeneration by migrating toward the periinfarct area and acquiring the neuron-specific receptor function," reports the Journal of Nuclear Medicine.
Department of Neurosurgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and 2Research and Development Division, Research Center, Nihon Medi-Physics Co. Ltd., Sodegaura, Japan.
Recent studies have indicated that bone marrow stromal cells (BMSC) have the potential to improve neurologic function when transplanted into animal models of central nervous system disorders. However, how the transplanted BMSC restore the lost neurologic function is not clear. In the present study, therefore, we aimed to elucidate whether BMSC express the neuron-specific gamma-aminobutyric acid (GABA) receptor when transplanted into brain that has been subjected to cerebral infarction. METHODS: The BMSC were harvested from green fluorescent protein-transgenic mice and were cultured. The mice were subjected to permanent middle cerebral artery occlusion. The BMSC or vehicle was transplanted into the ipsilateral striatum 7 d after the insult. Using autoradiography and fluorescence immunohistochemistry, we evaluated the binding of (125)I-iomazenil and the expression of GABA receptor protein in and around the cerebral infarct 4 wk after transplantation. RESULTS: Binding of (125)I-iomazenil was significantly higher in the periinfarct neocortex in the BMSC-transplanted animals than in the vehicle-transplanted animals. Likewise, the number of the GABA(A) receptor-positive cells was significantly higher in the periinfarct neocortex in the BMSC-transplanted animals than in the vehicle-transplanted animals. A certain subpopulation of the transplanted BMSC expressed a neuron-specific marker, microtubule-associated protein 2, and the marker protein specific for GABA(A) receptor in the periinfarct area. CONCLUSION: These findings suggest that BMSC may contribute to neural tissue regeneration through migrating toward the periinfarct area and acquiring the neuron-specific receptor function.
