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Background  Kisspeptin‐10 ( KP ‐10), a potent vasoconstrictor and inhibitor of angiogenesis, and its receptor,  GPR 54, have currently received much attention in relation to pre‐eclampsia. However, it still remains unknown whether  KP ‐10 could affect atherogenesis.    Methods and Results  We evaluated the effects of  KP ‐10 on human umbilical vein endothelial cells, human monocyte‐derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E–deficient (ApoE −/− ) mice in vivo.  KP ‐10 significantly increased the adhesion of human monocytes to human umbilical vein endothelial cells, which was significantly inhibited by pretreatment with P234, a  GPR 54 antagonist.  KP ‐10 stimulated  mRNA  expression of tumor necrosis factor‐α, interleukin‐6, monocyte chemotactic protein‐1, intercellular adhesion molecule‐1, vascular adhesion molecule‐1, and E‐selectin in human umbilical vein endothelial cells.  KP ‐10 significantly enhanced oxidized low‐density lipoprotein–induced foam cell formation associated with upregulation of  CD 36 and acyl‐CoA:cholesterol acyltransferase‐1 in human monocyte‐derived macrophages. In human aortic smooth muscle cells,  KP ‐10 significantly suppressed angiotensin  II –induced migration and proliferation, but enhanced apoptosis and activities of matrix metalloproteinase ( MMP )‐2 and  MMP ‐9 by upregulation of extracellular signal‐regulated kinase 1 and 2, p38, Bcl‐2‐associated X protein, and caspase‐3. Four‐week‐infusion of  KP ‐10 into ApoE −/−  mice significantly accelerated the development of aortic atherosclerotic lesions with increased monocyte/macrophage infiltration and vascular inflammation as well as decreased intraplaque vascular smooth muscle cells contents. Proatherosclerotic effects of endogenous and exogenous  KP ‐10 were completely canceled by P234 infusion in ApoE −/−  mice.    Conclusions  Our results suggest that  KP ‐10 may contribute to accelerate the progression and instability of atheromatous plaques, leading to plaque rupture. The  GPR 54 antagonist may be useful for prevention and treatment of atherosclerosis. Thus, the  KP ‐10/ GPR 54 system may serve as a novel therapeutic target for atherosclerotic diseases.

Potent Vasoconstrictor Kisspeptin‐10 Induces Atherosclerotic Plaque Progression and Instability: Reversal by its Receptor GPR 54 Antagonist