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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 2. Platelet-derived HMGB1 suppresses monocyte apoptosis.

Figure 2

Preincubation of monocytes with CM derived from CRP-activated or ADP-activated, but not resting platelets reverses the effect of staurosporine on monocyte mitochondrial transmembrane potential (TMRE) (A) and Annexin V-binding (B). (C,D) The addition of a neutralizing anti-HMGB1 antibody to CM derived from CRP-activated or ADP-activated platelets reverses the antiapoptotic effects. (E) In immunofluorescence stainings and confocal laser scanning microscopy, intracellular cleaved caspase-3 is upregulated in ABT-737-treated apoptotic monocytes, which is suppressed by CM derived from CRP-activated platelets. In the presence of a neutralizing HMGB1 specific antibody, the effect exerted by the platelet media is markedly reversed. (F) CM derived from activated, but not resting platelets from HMGB1 Flox control mice increases TMRE fluorescence in ABT-737-treated and staurosporine-treated apoptotic monocytes, which is reversed when CM derived from HMGB1-deficient activated platelets is used. Data are presented as mean ± SD for N≥4 and at least three separate experiments in all studies. * p<0.05, ** p<0.01 (Student’s t test).