p-selectin is located on chromosome 1q21-q24, spans > 50 kb and contains 17 exons in humans. p-selectin is constitutively expressed in megakaryocytes (the precursor of platelets) and endothelial cells. p-selectin expression is induced by two distinct mechanisms. first, p-selectin is synthesized by megakaryocytes and endothelial cells, where it is sorted into the membranes of secretory granules. when megakaryocytes and endothelial cells are activated by agonists such as thrombin, p-selectin is rapidly translocated to the plasma membrane from granules. secondly, increased levels of p-selectin mrna and protein are induced by inflammatory mediators such as tumor necrosis factor-a (tnf-a), lps, and interleukin-4 (il-4). although tnf-a and lps increase levels of both mrna and protein in murine models, they do not appear to affect mrna in human endothelial cells, while il-4 increases p-selectin transcription in both species. the elevated synthesis of p-selectin may play an important role in the delivery of protein to the cell surface. in ischemic stroke patients, plasma p-selectin concentration was reported to be highly correlated to plasminogen activator inhibitor-1 activity and tissue plasminogen activator activity.