A lot of work has been done in the state of Michigan on stem cells. The University of Michigan and prestigious hospitals such as the Henry Ford Hospital and many others have been working on human stromal cells and stem cells, finding out ways in which they can be used as potential life-saving cures and treatments. Much work has been carried out to improve the outcome after stroke, traumatic brain injury, and cancer.
The laws in the state of Michigan with regard to stem cell research are different from those in other states. Michigan law bans any research that destroys embryos for nontherapeutic purposes. Michigan law also bans the use of the somatic cell nuclear transfer procedure. Many of the states that have enacted legislation prohibiting human cloning have distinguished between reproductive and therapeutic cloning, but Michigan does not. Michigan, like South Dakota, forbids therapeutic cloning.
Michigan Citizens for Stem Cell Research and Cures is a nonprofit organization formed to educate the citizens of the state of Michigan, including public officials and policy makers, about the complex science, the biomedical potential, and the current policies affecting stem cell research in Michigan to promote informed decision making on this important issue.
In 2000 the researchers at the Henry Ford Health Sciences Center Department of Neurology tested a hypothesis and found that intracerebral grafting of a combination of bone marrow (BM) with brain-derived neurotrophic factor enhances differentiation of BM cells and significantly improves motor recovery. Because most of the active studies involve rats, before involving human beings, fresh BM was harvested from adult rats. It was anticipated that this may provide a powerful autoplastic therapy for human neurological injury and degenerative disorders.
In 2001 a significant step was taken by the Department of Neurosurgery at the Henry Ford Health Sciences Center. Rats were subjected to traumatic brain injury (TBI), and marrow stro-mal cells (MSCs) were injected into the tail vein 24 hours after TBI.
The rats were killed 15 days later. It was found that MSCs injected intravenously significantly reduced motor and neurological deficits. On the basis of this data, the researchers suggested that the intravenous administration of marrow stromal cells may be a promising therapeutic strategy that may be useful in treating TBI and that warrants further investigation.
The same year, researchers tested the hypothesis that intravenous infusion of bone marrow-derived MSCs enter the brain and reduce neurological functional deficits after stroke in rats. Significant recovery of somatosensory behavior was found. To test the efficacy of various delivery routes of stem cells, the researchers injected MSCs into the internal carotid artery of the adult rat after TBI. They came up with the suggestion that intra-arterial transplantation of MSCs along with intravenous and intracerebral transplantation is also a viable route for the administration of MSCs for the treatment of TBI, as MSCs infused intra-arterially after TBI survive and migrate into the brain.
As human umbilical cord blood cells (HUCBC) are rich in stem and progenitor cells, a team of researchers went ahead and tested whether intravenously infused HUCBC could enter the brain, survive, differentiate, and improve neurological functional recovery after stroke in rats. In addition, it was also tested whether ischemic brain tissue extract selectively induces chemotaxis of
HUCBC in vitro. Treatment with HUCBC significantly improved functional recovery, and significant HUCBC migration activity also was present. Therefore, HUCBC transplantation may provide a cell source to treat stroke.
The specific mechanisms by which introduced MSCs provide benefit remain to be elucidated. Various growth factors have been shown to mediate the repair and replacement of damaged tissue. Vascular endothelial growth factor (VEGF) is a growth factor responsible for growth of new vessels. It was confirmed that intravenous infusion of human bone marrow stromal cells promotes VEGF secretion, VEGF receptor 2 expression, and angiogenesis in the ischemic boundary zone of the host brain after stroke.
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