The mbKitL is expressed in vivo by inflamed endothelium and by neointima vessels. (A) RQ-PCR was performed on ECs derived from normal vessels or from different grade of atherosclerotic plaques. GUS gene was used to normalize the samples. (B) EPCs were let to adhere to ECs derived from normal or atherosclerotic vessels. In selected experiments, ECs from atherosclerotic plaques were pretreated with anti-KitL or EPCs were pretreated with K44. Adherent cells were counted and statistical analysis was performed (data are the mean ± SD; *P < .05 control vs experimental group: §P < .05 ECs from atherosclerotic vessels + anti-KitL or + K44 vs ECs from atherosclerotic vessels). (C) Specimens from normal vessels or atherosclerotic lesions were double immunostained with an anti-KitL or an anti-CD31 as primary antibody. TRITC- or FITC-conjugated goat anti–mouse IgG was used as secondary antibody, respectively. Colocalization of mbKitL and CD31 is represented in merge. Arrows indicated atherosclerotic vessels. Similar results were obtained with 6 different samples. (D) Representative immunofluorescence microscopy of Matrigel plugs containing human microvascular endothelial cells and TNFα (20 ng/mL) is reported. An anti-KitL or an anti-CD31 antibody was used as primary antibody. TRITC- or FITC-conjugated IgG was used as secondary antibody, respectively. Colocalization of mbKitL and CD31 in neoformed vessels is reported in merge. Four different sections per mice (4 mice) were analyzed.