“…25 TM, a 557-amino-acid type I transmembrane protein on the endothelium, binds exosite I on thrombin to alter thrombin specificity toward protein C. 29 The thrombin-TM complex activates protein C and thrombin-activatable fibrinolysis inhibitor, 30 thus inhibiting thrombus formation 31 and complement activation. 32 Under certain pathologic conditions, such as acute inflammation, 33,34 hyperglycemia, 35,36 endotoxemia, 37 ischemia-reperfusion injury, 33,38 and bypass surgery, 39,40 or stimulation with tumor necrosis factor a 41,42 and atrial natriuretic peptide, 43 the ectodomains of Sdc-1 and TM are cleaved by leukocyte-derived proteases, metalloproteinases, and heparinase. Therefore, increased plasma levels of Sdc-1 have been observed in patients with inflammation, 40 sepsis, 44 traumatic brain injury, 38 hemorrhagic shock, 45 disseminated intravascular coagulation (DIC), 46 and respiratory failure.…”