Publications by authors named "Jainwei Zhang"
Antiphospholipid Abs (APLAs) are associated with thrombosis and recurrent fetal loss. These Abs are primarily directed against phospholipid-binding proteins, particularly β(2)GPI, and activate endothelial cells (ECs) in a β(2)GPI-dependent manner after binding of β(2)GPI to EC annexin A2. Because annexin A2 is not a transmembrane protein, the mechanisms of APLA/anti-β(2)GPI Ab-mediated EC activation are uncertain, although a role for a TLR4/myeloid differentiation factor 88-dependent pathway leading to activation of NF-κB has been proposed.
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- Beta(2)-glycoprotein I (beta(2)GPI) enhances the activation of plasminogen by tissue plasminogen activator (tPA), which is crucial for regulating fibrin breakdown in the body.
- The study employed various assays to demonstrate that beta(2)GPI binds tPA and significantly improves its efficiency in converting plasminogen to plasmin, indicating its role in promoting fibrinolysis.
- Anti-beta(2)GPI antibodies, especially those from patients with antiphospholipid syndrome, can hinder this stimulating effect, potentially increasing the risk of thrombosis.