Cells that are chronically exposed to inflammatory signals are more prone to aging than those which are not exposed to such signals. Human vascular endothelial cell (HUVEC) primary cultures activated with TNF-alpha probably increase the expression of ICAM and VCAM, synthesize ROS, and express senescence markers. It is not known what the principal intracellular pathway is (although it is thought that STAT may play a role) and it is unknown if one or more proinflammatory cytokines are needed to activate NF-KB. We are trying to find out the role that IFN-alpha and/or IL-6 and IL-1B may have on the aging inflammatory phenomena and we aim at detecting the intracellular signal pathways (STAT). We are also working on the characterization of the genes involved in these abnormal biologic responses.

Cellular microparticles (CMP) are released depending on the activation and/or the presence of cell apoptosis. They are capable of activating both inflammatory and coagulation pathways. It seems that levels of CMP are higher in healthy pregnant women. A working hypothesis establishes that an increase of CMP levels may be found in recurrent pregnancy loses and preeclampsia. It is thought that their thrombophilic capacity may be higher in those patients with anti-phospholipid antibodies, especially among those with lupus anticoagulant. We want to determine MPC levels in non-pregnant healthy women, pregnant women without previous abnormal obstetric events, women with recurrent pregnancy loses, and women with severe preeclampsia. We are also evaluating whether there are differences related to the presence or absence of antiphospholipid antibodies. Finally, we will also characterize the exact type of CMP (endothelial, platelet-like, leuco-monocyte, and throphoblastic).

Three to five percent of pregnancies are complicated by preeclampsia (PE). PE is a multisystemic-related endothelial dysfunction disorder characterized by hypertension, proteinuria and renal injury. Despite considerable research, its etiology and pathophysiology still remains unclear. Different theories involving many pathways including thrombophilia, immunologic changes, circulating angiogenic /antiangiogenic factors and increased oxidative stress have been related to its pathogenesis. The role played by antiphospholipid antibodies (aPL) is a matter of discussion in PE.  Biological evidence of endothelial dysfunction related to PE/FGR has been shown by modified plasma markers including fibronectin, von Willebrand factor and ICAM-1 in a similar manner to that which occurs in aPL-related obstetric complications. We are searching now the role played by different aPL and cofactor antibodies, as well as its relationship with angiogenic /antiangiogenic factors and microparticle number in severe PE.

Three to five percent of pregnancies are complicated by preeclampsia (PE). PE is a multisystemic-related endothelial dysfunction disorder characterized by hypertension, proteinuria and renal injury. Despite considerable research, its etiology and pathophysiology still remains unclear. Different theories involving many pathways including thrombophilia, immunologic changes, circulating angiogenic /antiangiogenic factors and increased oxidative stress have been related to its pathogenesis. The role played by antiphospholipid antibodies (aPL) is a matter of discussion in PE.  Biological evidence of endothelial dysfunction related to PE/FGR has been shown by modified plasma markers including fibronectin, von Willebrand factor and ICAM-1 in a similar manner to that which occurs in aPL-related obstetric complications. We are searching now the role played by different aPL and cofactor antibodies, as well as its relationship with angiogenic /antiangiogenic factors and microparticle number in severe PE.