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Abnormal monocyte recruitment and collateral artery formation in monocyte chemoattractant protein-1 deficient mice

Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands

Imo E Hoefer

Research Group for Experimental and Clinical Arteriogenesis at the Department of Cardiology and Angiology, Albert-Ludwigs University Freiburg, Germany

Niels van Royen

Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands, Research Group for Experimental and Clinical Arteriogenesis at the Department of Cardiology and Angiology, Albert-Ludwigs University Freiburg, Germany

Jing Hua

Research Group for Experimental and Clinical Arteriogenesis at the Department of Cardiology and Angiology, Albert-Ludwigs University Freiburg, Germany

Stijn de Graaf

Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands

Christoph Bode

Research Group for Experimental and Clinical Arteriogenesis at the Department of Cardiology and Angiology, Albert-Ludwigs University Freiburg, Germany

Ivo R Buschmann

Research Group for Experimental and Clinical Arteriogenesis at the Department of Cardiology and Angiology, Albert-Ludwigs University Freiburg, Germany

Jan J Piek

Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands, j.j.piek{at}amc.uva.nl

Monocyte chemoattractant protein 1 (MCP-1) has been shown to be effective for the stimulation of collateral artery formation in small and large animal models. The availability of a genetic knockout mouse enables evaluation of the importance of the role of MCP-1 in the natural course of collateral artery growth. In a total of 21 MCP-1 = as well as 13 of the appropriate genetic background controls (f129Sv=JXC57Bl=6JgF1), a femoral artery ligation was performed. Subsequently, a polyethylene catheter, connected to an osmotic minipump, was inserted retrogradely into the occluded femoral artery with the tip pointing upstream. Using this technique, PBS (MCP-1 =: n ¹/4-13 and C57Bl=6J: n ¹/4-13) or MCP-1 (JE; MCP-1 =: n ¹/4-8) was delivered intra-arterially. Seven days after ligation, determination of hind limb flow was assessed by controlled tissue perfusion using differently labeled fluorescent microspheres. MCP-1 = mice exhibited a reduction of hind limb flow of 32.9-9.2% of the unligated hind limb, compared with 55.4-6.8% in C57Bl=6J mice (p <0.01). MCP-1= mice that underwent a subsequent ‘rescue’ treatment with MCP-1 showed a restoration of flow to a level of 47.4-9.8% (p ¹/4 NS compared with PBS-treated C57Bl/6J). Specific immunohistochemical staining for monocytes (MOMA-2: MCP-1 =, n ¹/4-5 and C57Bl/6J, n ¹/4-5) showed a reduced number of monocytes around developing collateral arteries in the MCP-1 = mice. In conclusion, our data show that the absence of MCP-1 causes a strong reduction in flow restoration after femoral artery occlusion, coinciding with a reduced monocyte attraction, emphasizing the central role of this chemokine in the multifactorial process of collateral artery formation.

Key Words: collateral circulation • cytokines • macrophages • regional blood flow

Vascular Medicine, Vol. 9, No. 4, 287-292 (2004)
DOI: 10.1191/1358863x04vm571oa


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