Effects of local MCP-1 protein therapy on the development of the collateral circulation and atherosclerosis in Watanabe hyperlipidemic rabbits

Royen, Niels van; Hoefer, Imo E.; Buschmann, Ivo; Kostin, Sawa; Voskuil, Michiel; Bode, Ch.; Schäper, Wolfgang; Piek, Jan J.

doi:10.1016/s0008-6363(02)00615-6

Cited by 67 publications

(45 citation statements)

References 27 publications

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“…In a rabbit model of hind-limb ischemia, local instillation of MCP-1 increased monocyte/macrophage recruitment, collateral vessel formation, and blood flow to the ischemic tissue. 67,68 After ligation of the femoral artery, CCR2 Ϫ/Ϫ mice had impaired distal blood flow and collateral artery formation, as compared with wild-type mice. 69 However, this impairment was largely limited to mice on the Balb/c genetic background.…”

Section: Arteriogenesismentioning

confidence: 99%

Chemokines in the Pathogenesis of Vascular Disease

Charo

Taubman

2004

Circulation Research

671

511

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Abstract-Our increasing appreciation of the importance of inflammation in vascular disease has focused attention on the molecules that direct the migration of leukocytes from the blood stream to the vessel wall. In this review, we summarize roles of the chemokines, a family of small secreted proteins that selectively recruit monocytes, neutrophils, and lymphocytes to sites of vascular injury, inflammation, and developing atherosclerosis. Chemokines induce chemotaxis through the activation of G-protein-coupled receptors, and the receptors that a given leukocyte expresses determines the chemokines to which it will respond. Monocyte chemoattractant protein 1 (MCP-1), acting through its receptor CCR2, appears to play an early and important role in the recruitment of monocytes to atherosclerotic lesions and in the formation of intimal hyperplasia after arterial injury. Acute thrombosis is an often fatal complication of atherosclerotic plaque rupture, and recent evidence suggests that MCP-1 contributes to thrombin generation and thrombus formation by generating tissue factor. Because of their critical roles in monocyte recruitment in vascular and nonvascular diseases, MCP-1 and CCR2 have become important therapeutic targets, and efforts are underway to develop potent and specific antagonists of these and related chemokines. A preponderance of evidence from clinical and experimental studies supports the notion that inflammation plays an important role in a wide range of cardiovascular diseases [1][2][3][4] and has focused attention on the signals that initiate cellular infiltration of vascular tissues. The chemokines are a family of potent chemotactic cytokines that regulate the trafficking of leukocytes and are rapidly upregulated at sites of vascular inflammation. Here, we review the role of monocyte chemoattractant protein 1 (MCP-1) and related chemokines in regulating the recruitment of monocyte/macrophages to the vessel wall and discuss how these chemokines contribute to the pathophysiology of vascular disease, with an emphasis on atherosclerosis. Chemokines and Chemokine ReceptorsChemokines (chemotactic cytokines) are small heparinbinding proteins that direct the migration of circulating leukocytes to sites of inflammation or injury. 5,6 There are Ϸ50 human chemokines, which are divided into three major families based on differences in their structure and function.The largest family is known as the CC chemokines because the first two of the four conserved cysteine residues that are characteristic of chemokines are adjacent to each other. CC chemokines tend to attract mononuclear cells and are found at sites of chronic inflammation. The most thoroughly characterized CC chemokine is MCP-1 (also known as CCL2), a potent agonist for monocytes, memory T cells, and basophils. The third family, the CX3C family, has only one known member, fractalkine (FK; or CX3CL1). FK consists of a soluble chemokine domain fused to a mucin-like stalk and a transmembrane domain. Thus, unlike other soluble chemokines, it is a type 1 tran...

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Section: Arteriogenesismentioning

confidence: 99%

Chemokines in the Pathogenesis of Vascular Disease

Charo

Taubman

2004

Circulation Research

671

511

View full text Add to dashboard Cite

show abstract

“…39 It also plays a role in collaterogenesis, an effect mediated through its recruitment of monocytes. 10 Further confirmation of the dual Janus-compatible effects of MCP-1, which would be anticipated given the role of the monocyte/macrophage in both atherogenesis and collaterogenesis, is the demonstration that infusing MCP-1 protein simultaneously enhances collaterogenesis in the ischemic hindlimb of apolipoprotein E (apoE)-knockout mice and increases atherosclerotic lesion size. 10 IFN-␥ illustrates how the Janus phenomenon can be a hypothesis-generating tool (Table 2 41,42 ).…”

Section: Inflammation In Atherogenesis and In Collaterogenesismentioning

confidence: 94%

“…10 Further confirmation of the dual Janus-compatible effects of MCP-1, which would be anticipated given the role of the monocyte/macrophage in both atherogenesis and collaterogenesis, is the demonstration that infusing MCP-1 protein simultaneously enhances collaterogenesis in the ischemic hindlimb of apolipoprotein E (apoE)-knockout mice and increases atherosclerotic lesion size. 10 IFN-␥ illustrates how the Janus phenomenon can be a hypothesis-generating tool (Table 2 41,42 ). Although evidence indicating an atherogenic effect of IFN-␥ is strong, 41,42 no definitive evidence indicates a collaterogenic effect.…”

Section: Inflammation In Atherogenesis and In Collaterogenesismentioning

confidence: 94%

“…Table 1 lists a few molecules for which reasonable evidence exists relating to both their atherosclerotic and collaterogenic effects and the actions of which are compatible with the Janus phenomenon. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] Complementary to the information contained in Table 1 are the opposite concordances displayed by different mouse strains regarding collaterogenic potential versus atherogenic susceptibility. C57BL/6 mice are susceptible to atherosclerosis and are exuberant collateral formers.…”

mentioning

confidence: 85%

“…Table 3 lists studies that relate to the possible Janus-like effects of different cell types. 10,23,28,53,[65][66][67][68][69][70][71][72][73][74][75] Of interest, the results of a recent, very small clinical trial were compatible with a Janus-like effect of progenitor cells on restenosis. The study was designed to examine the collaterogenic effects of intracoronary infusion of peripheral blood stem cells mobilized with granulocyte-colony stimulating factor in patients with acute myocardial infarction.…”

Section: Progenitor Cells In Atherogenesis and In Collaterogenesismentioning

confidence: 99%

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