A high-cholesterol diet induces increased SDF-1 plasma levels, favors CXCR4+ cell mobilization to PB, and favors HC migration toward SDF1. (A) Hypercholesterolemia is accompanied by an increase in PB plasma SDF-1 levels, as determined by ELISA quantification. (B) Flow cytometry analysis using Sca1/c-Kit (progenitor), CD19 (lymphocyte), and Gr-1 (neutrophils) cell-surface markers together with CXCR4 shows reduced numbers of double-positive cells per femur (×106) for all cell lineages tested. (C) Flow cytometry analysis with Lin−Sca1+c-Kit+ (progenitor), CD19+ (lymphocyte), and Gr-1+ (neutrophil) cell-surface markers together with CXCR4 shows increased numbers of double-positive B lymphocytes, neutrophils, and progenitor cells (× 104) in the PB of high-cholesterol mice. (D) LDL exposure (100 μg/mL) increased SDF-1 production by HUVEC in vitro, as determined by ELISA (*P < .05). These data were obtained from 3 separate experiments in which we used 6 mice per experimental condition with consistent results. (E) LDL (100 μg/mL) induces and HDL (100 μg/mL) reduces progenitor cells (Lin−Sca1+ c-Kit+) migration toward SDF-1. (F) LDL (100 μg/mL) induced B-lymphocyte (CD19+) migration toward SDF-1 is reversed when SR-BI is inhibited. LDL effect is reverted when SR-BI is inhibited (*P < .05). The data are shown as the number of migrating cells in relation to the control condition (SDF-1 alone). These data were obtained from 2 separate experiments with consistent results. CTR, control.
