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. Author manuscript; available in PMC: 2017 Sep 9.
Published in final edited form as: Biochem Biophys Res Commun. 2016 Jul 20;478(1):143–148. doi: 10.1016/j.bbrc.2016.07.078

Figure 1. Platelet-derived HMGB1 mediates monocyte recruitment via RAGE.

Figure 1

(A) In transwell migration experiments, monocytes migrate towards CM derived from CRP-activated and ADP-activated platelets. CM derived from resting platelets or the platelet agonists themselves only have moderate effects on monocyte recruitment. (B) Substantial amounts of HMGB1 are detected in CM derived from CRP-activated and ADP-activated platelets using ELISA. (C) Migration of monocytes towards CM of CRP-activated or ADP-activated platelets is altered in the presence of a neutralizing anti-HMGB1 antibody. (D) Preincubation of monocytes with a blocking antibody against RAGE inhibits monocyte migration towards CM of CRP-activated and ADP-activated platelets. (E) Monocytes migrate towards CM derived from CRP-activated and ADP-activated platelets from HMGB1 Flox control mice, which is inhibited when CM of activated platelets derived from HMGB1 PF4 mice is used. (F) Substantial amounts of HMGB1 are detected in CM derived from CRP-activated and ADP-activated platelets from HMGB1 Flox control mice. HMGB1 levels are decreased in CM of activated HMGB1 PF4 platelets. (G) In a trauma/hemorrhagic shock model, F4/80-positive macrophage infiltrates are detected in the liver and lung of HMGB1 Flox control mice, which are attenuated in HMGB1 PF4 mice. Data are presented as mean ± SD for N≥3 and at least three separate experiments in all studies. * p<0.05, ** p<0.01, *** p<0.001 (Student’s t test).