Skip to main content
Figure 2 | Journal of Inflammation

Figure 2

From: Upregulation of prolylcarboxypeptidase (PRCP) in lipopolysaccharide (LPS) treated endothelium promotes inflammation

Figure 2

PRCP-dependent prekallikrein (PK) activation and bradykinin (BK) liberation on LPS-treated HUVEC. Untreated, LPS-pretreated, or PRCP-siRNA transfected cells pretreated with LPS were incubated with 100 nM HK alone or in the presence of 1 μM HKH20 in HEPES buffer containing 2 mM Ca2+ and 1 mM Mg2+ at 37°C for 60 min. Afterward, 100 nM PK with 1 μM lisinopril [angiotensin-converting enzyme inhibitor (ACE)] and 1 μM HOE 140 (bradykinin B2 receptor antagonist) was added and incubated with HUVEC at 37°C for 60 min in the same buffer. Forty-eight hours after transfection with 100 nM PRCP-siRNA or control, cells were incubated with HK and PK and assessed for BK generation as described above. After PK activation on HUVEC, the buffer from each of the wells was collected and deproteinized by treatment with trichloroacetic acid. The data are from three experiments (means ± SEM).

Back to article page