The late clinical manifestations that arise when bioimplants are applied seem to have an immunologic basis. We are studying both the histological characteristics and the lesional mechanisms of the most frequently used implants. We try to analyze the role that bacteria may have in the induction and/or maintenance of these reactions and the possible correlation between particular HLA haplotypes and the adverse effects.

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).

Identification at the molecular level of pathways and proteins associated with the senescence of endothelial cells linked to aging and inflamatory responses. New candidate targets for therapeutic intervention at the clinical level and as new molecular moieties for nanomedicine approaches to improve aging related pathologies caused by endothelial inflamatory based senescence.

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.