The influence of differently structured nucleic acid compounds on PF4 binding to platelets is shown. (For details of the nucleic acid constructs, please compare with Figure 1B-F.) Enhancement of PF4 binding is expressed as the x-fold increase compared with PF4 binding to platelets in buffer only. Heparin (gray line) was used as the positive control. (A) PF4 binding to platelets was performed in the presence of increasing doses of cellular RNA (▪). Pretreatment with RNase A (□) significantly reduced PF4 binding to platelets (P = .0037). (B) PF4 binding to platelets was evaluated in the presence of increasing doses of nucleic acids with different lengths: 45mer–double-stem-loop RNA II (▲), 21mer–hairpin RNA (○), and 10mer–single-stranded DNA (♦). (C) PF4 binding to platelets was performed with increasing doses of 45mer–nucleic acid compounds, comprising different structures: 45mer–double-stem-loop RNA I (▪), 45mer–double stem-loop DNA (△), 45mer–polyA (●), 45mer–polyC (♦), and single nucleotides (□). (D) PF4 binding to platelets was measured in the presence of increasing doses of double-stranded vs single-stranded 21mer–DNA compounds: 21mer–double-stranded DNA (▪), 21mer–hairpin DNA (●), and 21mer–single-stranded DNA (□). Enhancement of PF4 binding is expressed as the x-fold increase of PF4 binding compared with platelets in buffer only. Negative values indicate detachment of PF4 from the platelet surface below the baseline value. All data represent mean ± SD of 3 independent experiments. ***P < .001.