Umbilical Cord Stem Cells Converted Into Brain Support Cells
For the first time ever, stem cells from umbilical cords have been converted into other types of cells, which may eventually lead to new treatment options for spinal cord injuries and multiple sclerosis, among other nervous system diseases. This is the first time this has been done with non-embryonic stem cells. Stem cells from umbilical cords do not pose an ethical dilemma because the cells come from a source that would otherwise be discarded. Another major benefit is that umbilical cells generally have not been found to cause immune reactions, which would simplify their potential use in medical treatments. Norepinephrine, along with other stem cell growth promoters, caused the umbilical stem cells to convert, or differentiate, into oligodendrocytes. However, that conversion only went so far. The cells grew but then stopped short of reaching a level similar to what's found in the human nervous system. This growth of oligodendrocytes, while crucial, is only a first step to potential medical treatments. There are two main options to pursue through further research. The first is that the cells could be injected into the body at the point of a spinal cord injury to promote repair.
Another intriguing possibility relates to multiple sclerosis and similar conditions. Multiple sclerosis is one of the holy grails for this kind of research. Oligodendrocytes produce myelin, which insulates nerve cells, making it possible for them to conduct the electrical signals that guide movement and other functions. Loss of myelin leads to multiple sclerosis and other related conditions such as diabetic neuropathy.The injection of new, healthy oligodendrocytes might improve the condition of patients suffering from such diseases.
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Insulin Therapy May Help Repair Atherosclerotic Lesions in Diabetic Patients
New research reveals that insulin applied in therapeutic doses selectively stimulates the formation of new elastic fibers in cultures of human aortic smooth muscle cells. These results advance the understanding of the molecular and cellular mechanisms of diabetic vascular disease. The study is published in the February issue of The American Journal of Pathology .The research endorses the use of insulin therapy for the treatment of atherosclerotic lesions in patients with type I diabetes, in which the induction of new elastic fibers would mechanically stabilize the developing plaques and prevent arterial occlusions. Primary insulin deficiency and decreased cellular sensitivity to insulin have been implicated in the pathogenesis of impaired healing processes, atherosclerosis and hypertension, all frequently observed in patients with both type I and type II diabetes. However, the possibility of a direct contribution of insulin to the cellular and molecular mechanisms that control the production of elastic fibers (elastogenesis) has not been explored. The researchers conducted a series of experiments to determine whether low therapeutic concentrations of insulin would promote the production of elastic fibers in cultures of human aortic smooth muscle cells.
Investigators found that insulin does in fact stimulate the deposition of elastic fibers in cultures of human aortic smooth muscle cells. The data demonstrated, for the first time, that low doses of insulin induce the elastogenic effect solely through the activation of insulin receptor and trigger the downstream activation of the P13K signaling pathway. The ultimate up-regulation of elastic fiber deposition by insulin is executed through two parallel mechanisms: the initiation of elastin gene expression and the enhancement of tropoelastin secretion.Importantly, the experimental data suggest that insulin-dependent initiation of the elastin gene transcription occurs after dissociation of the FoxO1 transcription factor from the specific domain identified within the elastin gene promoter. Also insulin may facilitate the transportation of tropoelastin into the secretory endosomes, where it can associate with S-GAL/EBP, the "chaperone" protein that enhances secretion. The discovery of the elastogenic action of insulin allows for better understanding of the pathologic mechanisms in which the lack of insulin, in diabetes type I, or insulin resistance, in diabetes type II, contribute to the development of hypertension and the rapid progression of atherosclerosis.Importantly, the results indicate that the discovered elastogenic effect of low concentrations (0.5-10 nM) of insulin is not restricted to the arterial smooth muscle cells. Thus, insulin also stimulates formation of elastic fibers by human skin fibroblasts and by myofibroblasts isolated from human hearts. These observations constitute a real novelty in the field of regenerative medicine and endorse 1) local application of small doses of insulin for ameliorating difficult healing of dermal wounds in diabetic patients and 2) systemic administration of insulin in patients after heart infarctions, in hope that insulin-induced elastic fiber deposition may alleviate formation of maladaptive collagenous scars in the myocardium.
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