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Blood, 15 February 2004, Vol. 103, No. 4, pp. 1296-1304.
Prepublished online as a Blood First Edition Paper on October 23, 2003; DOI 10.1182/blood-2002-05-1480.
Submitted May 20, 2002
Accepted September 19, 2003
Chemokine receptor-8 (CCR8) mediates human vascular smooth muscle cell chemotaxis and metalloproteinase-2 secretion
Nasreen S Haque*, John T Fallon, Jiang Jin Pan, Mark B Taubman, and Peter C Harpel
Department of Medicine, Mount Sinai Medical School, New York, NY, USA
* Corresponding author; email: nasreen.haque{at}mssm.edu.
The response of the arterial vascular wall to injury is characterized by vascular smooth muscle (VSMC) migration, a process requiring metalloproteinase production. This migration is induced by cytokines, however the agonists involved are not fully defined. The CC chemokine receptor 8 (CCR8) is expressed on monocytes and T-lymphocytes and is the sole receptor for the human CC chemokine CCL1 (I-309) and for the viral chemokine, vCCL1 (vMIP-1). We have reported that CCR8 is expressed on human umbilical vein endothelial cells (HUVECs) and mediates chemotaxis induced by CCL1. The conditioned medium from incubation mixtures of lipoprotein Lp(a) and HUVECs (LCM) contained CCL1 and stimulated both monocyte and HUVEC chemotaxis providing novel mechanisms for the atherogenicity of Lp(a). We now report that CCL1, vCCL1 and LCM stimulate chemotaxis of human VSMCs that is blocked by murine monoclonal antibody against CCR8 and by the G-protein inhibitor pertussis toxin. The effect of anti-CCR8 was specific as this antibody failed to effect the chemotaxis of VSMCs in response to CCL3 or by PDGF-BB. VSMCs contained CCR8 mRNA and CCR8 antigen co-precipitated with VSMC membranes. Antibodies against MMP-2 inhibited the CCL1-induced chemotaxis of VSMCs whereas anti-MMP-9 was less effective. CCL1 induced VSMC pro-metalloproteinase-2 (MMP-2) mRNA and protein secretion. Poxvirus MC148 inhibited the increase in MMP-2 induced by CCL1 documenting that CCR8 was the receptor responsible. In mouse femoral arteries, CCR8 and TCA3 antigen co-localized with VSMCs and were upregulated after injury. The induction of CCR8 and CCL1/TCA3 under conditions associated with VSMC proliferation and migration raises the possibility that CCR8 may play an important role in vessel wall pathology.
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