Monocytes belong to the most important mediators of arteriogenesis. Mice deficient (KO) for the transcription factor early growth response 1 (Egr-1) demonstrate impaired perfusion recovery after femoral artery occlusion (occ). Monocyte recruitment and perivascular accumulation is mediated by MCP-1 (monocytes chemoattractant protein-1), uPa (urokinase plasminogen activator) and ICAM-1 (intercellular adhesion molecules-1) – all of them presenting downstream genes of Egr-1. In our study we induced arteriogenesis in Egr-1 KO and their wild-type (WT) controls via occ. The left leg was sham operated. 3d after occ immunhistochemical staining for quantitative assessment of perivascular macrophage (MF) accumulation were performed. Results evidenced significantly increased amounts of perivascular MF (occ vs. sham) in WT and KO mice, showing even higher amounts of MF in occ KO vs. occ WT (8.2 vs. 5.4 per vessel, p<0.05). qRT-RNA results on mRNA expression-levels of MCP-1, ICAM-1 and uPa in growing collaterals revealed significantly increased levels of all three transcripts in KO and WT mice 12h after occ persisting in KO mice also at 24h when WT RNA levels had already equalized. A comparison of sham WT and KO mice revealed significantly fewer resident MF in KO than in WT mice (1.8 vs. 4.3 p.v., p<0.05) indicating impairment of baseline MF extravasation in KO mice. Accordingly, unligated KO mice showed a higher percentage of monocytes in peripheral blood samples as confirmed by FACS analyses. In summary our results indicate that MF recruitment and extravasation is strongly impaired under normal conditions. However, a strong stimulus like induction of arteriogenesis via occ induces overcompensation of Egr-1 functions resulting in persisting augmented levels of the Egr-1 downstream genes uPA, MCP-1 and ICAM-1. The mechanisms, however, probably mediated by other members of the Egr family, are not capable of promoting patent proliferation of growing collateral vessels.