Abstract
Increasing evidence suggests that infection and other proinflammatory agents upregulate bradykinin and kallikrein, thereby promoting the proinflammatory response. In this study, we focused on proinflammatory role of prolylcarboxypeptidase (PRCP) induced by lipopolysaccharide (LPS), which induces inflammatory kinins [bradykinin (BK)] and kallikrein on endothelial cells. PRCP activates prekallikrein (PK) to kallikrein leading to the generation of bradykinin (BK) from high molecular weight kininogen (HK). After treating endothelial cells with LPS at sublethal concentrations, the mRNA for PRCP and antigen increased. The generation of both kallikrein and BK were elevated by three fold, suggesting PRCP upregulation contributes to the risk of developing inflammation. This amplification might be an additional mechanism whereby PRCP promotes a sustained inflammatory response. The inhibitor of PRCP and PRCP siRNA effectively attenuated the increase in kallikrein and BK generation on LPS‐treated endothelial cells. Taken together, these findings indicate that LPS at sublethal concentrations enhances PRCP‐dependent PK activation in endothelial cells. This study was supported by American Heart Association 0330193N, NCRR/NIH P20RR021929, and NSF MRI 0619774 ZS
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