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Background  In order to identify factors that stimulate arteriogenesis after ischemia, we followed gene expression profiles in two extreme models for collateral artery formation over 28 days after hindlimb ischemia, namely “good‐responding” C57 BL /6 mice and “poor‐responding”  BALB /c mice.    Methods and Results  Although  BALB /c mice show very poor blood flow recovery after ischemia, most known proarteriogenic genes were upregulated more excessively and for a longer period than in C57 BL /6 mice. In clear contrast, chemokine genes  Ccl19 ,  Ccl21a , and  Ccl21c  and the chemokine receptor   CCR 7  were upregulated in C57 BL /6 mice 1 day after hindlimb ischemia, but not in  BALB /C mice.  CCL 19 and  CCL 21 regulate migration and homing of T lymphocytes via  CCR 7. When subjecting  CCR 7 −/− / LDLR  −/−  mice to hindlimb ischemia, we observed a 20% reduction in blood flow recovery compared with that in  LDLR  −/−  mice. Equal numbers of α‐smooth muscle actin–positive collateral arteries were found in the adductor muscles of both mouse strains, but collateral diameters were smaller in the  CCR 7 −/− / LDLR  −/− . Fluorescence‐activated cell sorter analyses showed that numbers of  CCR 7 +  T lymphocytes (both  CD 4 +  and  CD 8 + ) were decreased in the spleen and increased in the blood at day 1 after hindlimb ischemia in  LDLR  −/−  mice. At day 1 after hindlimb ischemia, however, numbers of activated  CD 4 +  T lymphocytes were decreased in the draining lymph nodes of  LDLR  −/−  mice compared with  CCR 7 −/− / LDLR  −/−  mice.    Conclusions  These data show that  CCR 7‐ CCL 19/ CCL 21 axis facilitates retention  CD 4 +  T lymphocytes at the site of collateral artery remodeling, which is essential for effective arteriogenesis.

CCR 7‐ CCL 19/ CCL 21 Axis is Essential for Effective Arteriogenesis in a Murine Model of Hindlimb Ischemia