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Knockdown of CCR1 suppresses expression of Intercellular Cell Adhesion Molecule‐1 induced by hypoxia/reoxygenation in endothelial cells and reduces infarct sizes after myocardinal ischemia/reperfusion

It has been reported that CCL15, a CCR1 ligand, induces proatherogenic factors and has been implicated in atherosclerosis. The present study showed that exposure of human endothelial cells (ECs) to hypoxia and reoxygenation (H/R) resulted in a rapid increase in expression of ICAM‐1 and CCR1 ligands. Our results revealed that knockdown of CCR1 attenuated expression of ICAM‐1 in ECs after H/R. Stimulation of ECs with CCL15 increased expression of ICAM‐1 compared with those in non‐stimulated cells predominantly via CCR1. Our data showed that CCL15 increased cell adhesion of monocytoid cells to endothelial cells. Pretreatment of these cells with CCR1 siRNA prevented the CCL15‐induced expression of ICAM‐1 and monocyte adhesion to ECs. We further investigated expression of CCR1 ligands and ICAM‐1 in vivo after myocardinal ischemia and reperfusion (MIR). Enhanced expression of ICAM‐1 and CCR1 ligands has been demonstrated in rat hearts in vivo after MI‐R. Direct injection of CCR1 siRNA onto the ventricular wall reduced expression of ICAM‐1 in rat hearts activated by MI‐R. Staining of hearts revealed that silencing of CCR1 markedly reduced the infarct sizes after MI‐R. Our results indicate that CCR1 and its ligands play important roles in inflammatory responses after MI/R via upregulating expression of cell adhesion molecules.