Células madre: una revolución en la medicina regenerativa / Stem cells: a revolution in regenerative medicine

Los avances en la medicina regenerativa han sido evidentes en los últimos años y esto se ha obtenido por los nuevos conocimientos alcanzados en relación con las células madre, cuyo uso en la terapia de reemplazo ha dado lugar a una nueva era en la medicina. A tales efectos se realizó una revisión bibliográfica con el objetivo de difundir sus generalidades y aplicaciones, así como lo relacionado con las investigaciones básicas que se realizan en ese campo y los principales logros obtenidos. La posibilidad de expansión y diferenciación de dichas células, permite obtener un número suficiente de estas, lo cual ayuda al desarrollo de la terapia celular

Advances in regenerative medicine have been evident in the last years and this has been obtained due to the new knowledge related to stem cells, which use in the replacement therapy has given rise to a new age in medicine. To such effects, a literature review was carried out aimed at spreading its generalities and implementations, as well as everything related to the basic investigations carried out in this field and the main achievements obtained. The possibility of expansion and differentiation of such cells, allow to obtain enough quantitiy of them, which helps the development of cell therapy

Stem cell factor protects against neuronal apoptosis by activating AKT/ERK in diabetic mice

Neuronal apoptosis occurs in the diabetic brain due to insulin deficiency or insulin resistance, both of which reduce the expression of stem cell factor (SCF). We investigated the possible involvement of the activation of the MAPK/ERK and/or AKT pathways in neuroprotection by SCF in diabetes. Male C57/B6 mice (20-25 g) were randomly divided into four groups of 10 animals each. The morphology of the diabetic brain in mice treated or not with insulin or SCF was evaluated by H&E staining and TUNEL. SCF, ERK1/2 and AKT were measured by Western blotting. In diabetic mice treated with insulin or SCF, there was fewer structural change and apoptosis in the cortex compared to untreated mice. The apoptosis rate of the normal group, the diabetic group receiving vehicle, the diabetic group treated with insulin, and the diabetic group treated with SCF was 0.54 ± 0.077 percent, 2.83 ± 0.156 percent, 1.86 ± 0.094 percent, and 1.78 ± 0.095 percent (mean ± SEM), respectively. SCF expression was lower in the diabetic cortex than in the normal cortex; however, insulin increased the expression of SCF in the diabetic cortex. Furthermore, expression of phosphorylated ERK1/2 and AKT was decreased in the diabetic cortex compared to the normal cortex. However, insulin or SCF could activate the phosphorylation of ERK1/2 and AKT in the diabetic cortex. The results suggest that SCF may protect the brain from apoptosis in diabetes and that the mechanism of this protection may, at least in part, involve activation of the ERK1/2 and AKT pathways. These results provide insight into the mechanisms by which SCF and insulin exert their neuroprotective effects in the diabetic brain.