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. 2014 Dec 1;190(11):1243–1254. doi: 10.1164/rccm.201406-1095OC

Figure 5.

Figure 5.

Receptor interacting serine/threonine-protein kinase 3 (RIP3) is released extracellularly after treatment with red blood cells (RBCs). (A) Lung endothelial cells (ECs) supernatant (SN) RIP3 is increased following treatment with RBCs; note the heterogeneity in RIP3 release induced by RBCs. (B) SN densitometry, P = 0.021, total of nine RBC units tested. (C) Lung EC RIP3 decreases following treatment with RBC, addition of necrostatin (Nec)-1–ZVAD attenuates loss of EC RIP3. (D) Supernatant RIP3 is increased following RBC treatment and attenuated with Nec-1, *P = 0.002, +P = 0.045.