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.

Angiotensin II, angiotensin receptors, apelins and recently de-orphanized APJ receptors are important control factors of cardiovascular system. The present studies aimed the effects of apelin-13 and [Pyr1]-apelin-13 on apoptosis of cultured rat vascular smooth muscle cells, induced by enhanced concentrations of angiotensin II, in the presence of losartan, a specific inhibitor of AT1 angiotensin receptors type. The obtained data demonstrated that apelin-13 was less efficient in preventing the apoptosis of aortic smooth muscle cells in culture, induced by angiotensin II (in the presence of losartan), as compared to [Pyr1]-apelin-13. It could be concluded that the apoptotic effects induced by angiotensin II in rat aortic could be related to the involvement of AT2 angiotensin receptor type, other types of receptors or pathways unrelated to angiotensin receptors. Furthermore, the apoptotic effects induced by angiotensin II are counteracted by apelins in a structure-related manner.