2 research outputs found
Platelet-activating anti-PF4 antibodies mimic VITT antibodies in an unvaccinated patient with monoclonal gammopathy
Transient prothrombotic disorders caused by plateletactivating antibodies against platelet factor 4 (PF4) include heparin-induced thrombocytopenia (HIT), spontaneous HIT syndrome,1 and, most recently, vaccine-induced immune thrombotic thrombocytopenia (VITT).2 Here, we identified prothrombotic, platelet-activating anti-PF4 antibodies, not associated with heparin treatment, in a patient with monoclonal gammopathy that resulted in a chronic hypercoagulability state. </p
Cardiovascular functions of Ena/VASP proteins: past, present and beyond
Actin binding proteins are of crucial importance for the spatiotemporal regulation of actin cytoskeletal dynamics, thereby mediating a tremendous range of cellular processes. Since their initial discovery more than 30 years ago, the enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) family has evolved as one of the most fascinating and versatile family of actin regulating proteins. The proteins directly enhance actin filament assembly, but they also organize higher order actin networks and link kinase signaling pathways to actin filament assembly. Thereby, Ena/VASP proteins regulate dynamic cellular processes ranging from membrane protrusions and trafficking, and cell-cell and cell-matrix adhesions, to the generation of mechanical tension and contractile force. Important insights have been gained into the physiological functions of Ena/VASP proteins in platelets, leukocytes, endothelial cells, smooth muscle cells and cardiomyocytes. In this review, we summarize the unique and redundant functions of Ena/VASP proteins in cardiovascular cells and discuss the underlying molecular mechanisms. </p