The present studies aimed the effects of tyrphostin AG 494 and tyrphostin AG 1295 on apoptosis of mouse pro-B lymphocytes. The actual scientific literature lacks such data. Tyrphostin AG 494 is an inhibitor of epidermal growth factor receptor pathways and tyrphostin AG 1295 is an inhibitor of platelet-derived growth factor receptor pathways. Our obtained data demonstrated that tyrphostin AG 1295 was less effective in preventing the apoptosis of murine pro-B cells, triggered by the combination of Cytoporone B (NR4A1 agonist) and Cyclosporine A. In contrast, tyrphostin AG 494 had a stronger inhibitory effect on the apoptosis of the same cells, when administered for 24 hours. Thus, when blocking the activation of epidermal growth factor receptor pathways, the inductive apoptotic effects of Cytoporone B and Cyclosporine A are reduced. Thus, we could conclude that such inhibition will increase the resistance to apoptosis of pro-B cells. Thus, such a resistance to apoptosis could be experimentally acquired by hematopoietic cells.
We tempted to explore the biochemical effects, represented by apoptosis, triggered by conditioned medium, obtained as a result of culturing mesenchymal stem cells for 24 h, on endothelial progenitor cells. The mesenchymal stem cells were developed on collagen fibers in the presence of thapsigargin, concanavalin A, leptin and ghrelin. Meanwhile, were used the following inhibitors: AG490, a JAK2 inhibitor; PD98059, a MEK/ERK inhibitor; and LY294002, a PI3K/Akt signaling inhibitor. When we analyzed the results, we observed that the conditioned medium, obtained from mesenchymal stem cells cultivation, applied in a 10% concentration for 24 H , induced apoptosis of endothelial progenitor cells in different degrees: 10 �M leptin] ghrelin]]concanavalin A @ apelin. Furthermore, LY294002 and AG490-conditioned medium of mesenchymal stem cells reduced the apoptotic effects induced by leptin on developed endothelial progenitor cells. The very first conclusion is that the inhibition of PI3K/Akt signaling pathway is blocking the apoptotic effects of leptin stimulation of mesenchymal stem cells population. The inhibition of JAK/STAT pathways seems to be less effective.
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