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Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid (aPL) antibodies - Guillermina Girardi

March 26, 2012

We developed a new animal model of TMA induced by antiphospholipid (aPL) antibodies, an invaluable tool to understand the molecular and cellular eventsthat determine glomerular endothelial injury. Using this model we found more than one mechanism/signaling pathway is involved in glomerular injury induced by aPL- antibodies. Both complement dependent and complement-independent pathways were identified that lead to glomerular endothelial cell damage and renal function impairment. We also found that C5a-C5aR interaction is a crucial step for the activation of the coagulation cascade and glomerular injury induced by complement activating antibodies. In addition, our studies demonstrated complement independent mechanisms in which reactivity with β2 glycoprotein I (β2GPI) plays an important role in aPL-induced glomerular damage and renal failure. Independently of the mechanism responsible for aPL-induced TMA, mice that express low levels of tissue factor (TF) were protected from glomerular injury.


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Source: Alliance for Lupus Research
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