Östrojen hormonunun apoptoz yolakları aracılığıyla mezenkimal kök hücrelerinin muhafaza edilmelerindeki etkisi

Mesenchymal Stem Cells (MSCs) can both self-renew and differentiate into fat,bone, cartilage, and muscle. They have a high therapeutic value due to theirdifferentiation potential and nonimmunogenic characteristics, however their rarenessand duration of their culture are the main handicaps in their application in cell-basedtherapies. Therefore, our aim was to explore the possible mechanisms that areinvolved in MSC maintenance and proliferation by using rat MSCs as a model. Westudied the effect of estrogen on MSCs due to its role in growth regulation,differentiation, and cellular proliferation. In MSCs isolated from both normal andovariectomized animals, the number and the CFU activity were increased whencultured with estrogen. To reveal the mechanism of the action of estrogen on MSCmaintenance, we investigated the apoptotic pathway since estrogen has been shownto have a detrimental effect on apoptosis in other systems. The number of apoptoticcells decreased when MSCs were cultured in the presence of estrogen. To elucidatethe molecular mechanism of estrogen?s effect on MSC apoptosis, we examined theexpression of the bcl-2 family of genes. The expression of anti- apoptotic Bcl-2 andBcl-xL proteins increased in the presence of estrogen, whereas the expression ofpro-apoptotic Bak decreased. Our results clearly show that estrogen increases thenumber of the functional MSCs by differentially regulating the expression of thebcl-2 family of genes and inhibiting apoptosis. Therefore estrogen treatment ofMSCs may offer a potential to increase the number of MSC for treatments.Keywords: Mesenchymal Stem Cells, estrogen, bcl-2 family of genes, rat