Figure 7
From: Kallistatin treatment attenuates lethality and organ injury in mouse models of established sepsis
Kallistatin treatment enhances suppressor of cytokine signaling-3 (SOCS3) expression through activation of a tyrosine kinase-protein kinase C (PKC)-extracellular signal-regulated kinase (ERK) signaling pathway in RAW264.7 cells. (A) Macrophages were incubated with 0.05 μM wild-type kallistatin (WT-KS), heparin-mutant kallistatin (HM-KS) or active site-mutant kallistatin (AM-KS) for 12 hours. Wild-type or heparin mutant kallistatin, but not active site mutant kallistatin, significantly increased SOCS3 expression (n = 3). (B) The effect of kallistatin on SOCS3 expression in macrophages was blocked by PD98059 (PD; ERK inhibitor), chelerythrine (CHE; PKC inhibitor) and genistein (GEN; tyrosine kinase inhibitor). (C) ERK phosphorylation induced by kallistatin in macrophages was also reversed by PD98059, chelerythrine and genistein (n = 3). *P <0.05 versus control group; # P <0.05 versus kallistatin alone.