Figure 3.

Apolipoprotein B‐100 (apoB‐100) fragmentation and expression of serum amyloid A (SAA)₄ in low‐density lipoprotein/very‐low‐density lipoprotein (LDL/VLDL) isolated from Porphyromonas gingivalis‐treated whole blood. Whole blood was incubated with P. gingivalis (5 × 10⁷ colony‐forming units [CFU]/mL, at 37°C, 30 minutes) wild‐type strains ATCC or W50, with the gingipain mutants E8 (lacking RgpA and RgpB) and K1A (lacking Kgp) or without bacteria (Control). LDL/VLDL was isolated from plasma by density/gradient‐ultracentrifugation and proteins were separated with 2‐dimensional gel electrophoresis (2DE) and silver stained (A). Two apoB‐100 fragments (7107: pI 7.2, Mr 20 kDa; and 7018: pI 7.9, Mr 15 kDa) and one SAA ₄ isoform (8104: pI 9.17, Mr 14.7 kDa) were identified by mass‐spectrometry analysis. B, The mean ± standard error of the mean spot optical density in parts per million (PPM) of total gel staining is presented from at least 4 independent experiments/subjects (n = 4‐6) (*P < .05, **P < .01, and ^t P ≤ .06). mut, mutant