Research Paper Volume 13, Issue 8 pp 10920—10933

Pentraxin-3-mediated complement activation in a swine model of renal ischemia/reperfusion injury

C1-inhibitor prevents PTX-3 binding on endothelial cells. (A) Frozen pig kidney sections were analyzed by indirect immunofluorescence to characterize the PTX3 source after 15 min of reperfusion in control and rhC1-INH treated pigs. PTX3 deposits were observed at the level of peritubular capillaries in control pigs. rhC1-INH infusion prevented PTX3 deposits on ECs. (B) FACS showed that ECs in basal condition did not bind both rhC1-INH and PTX3. Both PTX3 and rhC1-INH presented a significant binding on H2O2-activated ECs. When H2O2-activated EC were co-stimulated with PTX3 and rhC1-INH, rhC1INH prevented PTX3 binding. Results are representative of three independent experiments.

Figure 4. C1-inhibitor prevents PTX-3 binding on endothelial cells. (A) Frozen pig kidney sections were analyzed by indirect immunofluorescence to characterize the PTX3 source after 15 min of reperfusion in control and rhC1-INH treated pigs. PTX3 deposits were observed at the level of peritubular capillaries in control pigs. rhC1-INH infusion prevented PTX3 deposits on ECs. (B) FACS showed that ECs in basal condition did not bind both rhC1-INH and PTX3. Both PTX3 and rhC1-INH presented a significant binding on H2O2-activated ECs. When H2O2-activated EC were co-stimulated with PTX3 and rhC1-INH, rhC1INH prevented PTX3 binding. Results are representative of three independent experiments.