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

Voskuil, Michiel; Hoefer, Imo E.; Royen, Niels van; Hua, Jing; Graaf, S. de; Bode, Christoph; Buschmann, Ivo; Piek, Jan J.

doi:10.1191/1358863x04vm571oa

Cited by 52 publications

(46 citation statements)

References 24 publications

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“…7 Correspondingly, infusion of this chemokine into the proximal stump of an occluded femoral artery in rabbits markedly enhanced arteriogenesis, 25 whereas this was diminished in MCP-1 or CC chemokine receptor 2-deficient mice. 26,27 Despite its importance for the initiation of arteriogenesis, only little is known about the mechanisms that control the expression of MCP-1 in this context. Therefore, we subjected small second order branches of the mouse mesenteric artery to proarteriogenic flow conditions and identified the SMCs of the media as the main source of MCP-1.…”

Section: Discussionmentioning

confidence: 99%

Stretch-Induced Activation of the Transcription Factor Activator Protein-1 Controls Monocyte Chemoattractant Protein-1 Expression During Arteriogenesis

Demicheva

Hecker

Korff

2008

Circulation Research

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Abstract-Cerebral, coronary, and peripheral artery diseases combined represent the most frequent cause of death in developed nations. The underlying progressive occlusion of large conductance arteries can partially be compensated for by transformation of preexisting collateral arterioles to small artery bypasses, a process referred to as arteriogenesis. Because biomechanical forces have been implicated in the initiation of arteriogenesis, we have investigated the mechanosensitive expression of a pivotal proarteriogenic molecule, monocyte chemoattractant protein (MCP)-1, which governs the recruitment of circulating monocytes to the wall of the remodeling collateral arterioles. Using a new ear artery ligation model and the classic hindlimb ischemia model in mice, we noted that MCP-1 expression is significantly increased in collateral arterioles undergoing arteriogenesis already 24 hours after its onset. By mimicking proarteriogenic perfusion conditions in small mouse arteries, we observed that MCP-1 expression is predominantly upregulated in the smooth muscle cells, which solely sense changes in circumferential wall tension or stretch. Subsequent analyses of cultured endothelial and smooth muscle cells confirmed that cyclic stretch but not shear stress upregulates MCP-1 expression in these cells. Blockade of the mechanosensitive transcription factor activator protein-1 by using a specific decoy oligodeoxynucleotide abolished this stretch-induced MCP-1 expression. Likewise, topical administration of the decoy oligodeoxynucleotide to the mouse ear abrogated arteriogenesis through downregulation of MCP-1 expression and monocyte recruitment. Collectively, these findings point toward a stretch-induced activator protein-1-mediated rise in MCP-1 expression in vascular smooth muscle cells as a critical determinant for the initiation of arteriogenesis. T he combination of atherosclerosis in cerebral, coronary, and peripheral arteries and its sequelae represent the single most important cause of death in the industrialized world. Thrombotic occlusion of these large conductance arteries often causes severe ischemia in the affected tissues. Based on the clinical relevance of the disease, significant efforts have been made to offset its consequences by stimulating the growth of new blood vessels into the ischemic area. 1 However, angiogenesis per se is not sufficient to fully restore blood supply to the affected tissues. 2,3 Spontaneous enlargement of collateral arterioles to small arteries bypassing the occluded main artery, an adaptive remodeling process referred to as arteriogenesis, on the other hand, seems to be much more efficient in compensating for the consequences of atherosclerosis. 4,5 Morphologically, collateral arteriolar enlargement is associated with a corkscrew-like appearance that is the consequence of a growth in length between 2 fixed points. 6 On the molecular level, arteriogenesis is characterized by the upregulation of adhesion molecules such as intercellular adhesion molecule (ICAM)-1 and chemokines like...

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Section: Discussionmentioning

confidence: 99%

Stretch-Induced Activation of the Transcription Factor Activator Protein-1 Controls Monocyte Chemoattractant Protein-1 Expression During Arteriogenesis

Demicheva

Hecker

Korff

2008

Circulation Research

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“…28 -32 Conversely, animals deficient in MCP-1 or CCR2-chemokine receptor, an MCP-1 receptor, have been shown to display reduced monocyte/macrophage infiltration and collateral formation. 33,34 Previous work has indicated that OPN is an important mediator of macrophage adhesion and migration, and other studies have shown that OPN may be critical for macrophage infiltration into sites of injury in vivo. 15 In addition, two recent reports have indicated that OPN plays a key role in the regulation of the hematopoietic stem cell (HSC) niche in bone marrow.…”

Section: Duvall Et Al Osteopontin In Hind Limb Ischemia 293mentioning

confidence: 99%

The Role of Osteopontin in Recovery from Hind Limb Ischemia

Duvall

Weiss

Robinson

et al. 2008

ATVB

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Objective-Osteopontin (OPN) is a highly phosphorylated extracellular matrix glycoprotein that is involved in a diversity of biological processes. In the vascular wall, OPN is produced by monocytes/macrophages, endothelial cells, and smooth muscle cells, and it is thought to mediate adhesion, migration, and survival of these cell types. In this study, we hypothesized that OPN plays a critical role in recovery from limb ischemia. Methods and Results-We induced hind limb ischemia in wild-type and OPN Ϫ/Ϫ mice. OPN Ϫ/Ϫ mice exhibited significantly delayed recovery of ischemic foot perfusion as determined by LDPI, impaired collateral vessel formation as measured using micro-CT, and diminished functional capacity of the ischemic limb. In the aortic ring assay, normal endothelial cell sprouting was found in OPN Ϫ/Ϫ mice. However, OPN Ϫ/Ϫ peritoneal monocytes/macrophages were found to possess significantly reduced migration in response to chemoattraction. Conclusions-This

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“…9,30 Genetically modified mice deficient for either MCP-1 or CCR2 have an impaired monocyte response and less recovery of perfusion after interruption of arterial inflow. 12,13 In this study, the molecular signal for monocyte ␣ 5 -integrin at 4 days was markedly reduced in MCP-1 Ϫ/Ϫ mice compared with wild-type mice. The relatively mild differences in blood flow in the 2 groups was likely due to the early time interval (4 days).…”

Section: Discussionmentioning

confidence: 87%

“…Greater differences in flow would be expected at 7 to 21 days. 12,13 Interactions between VCAM-1 on the endothelium and integrins such as VLA-4 (␣ 4␤1 ) contribute to slow rolling and firm adhesion of monocytes and lymphocytes in the microcirculation. Targeted CEU in ischemic limbs detected VCAM-1 expression on the microvascular endothelium in a temporal pattern that paralleled monocyte ␣ 5 -integrin signal.…”

Section: Discussionmentioning

confidence: 99%

“…Beneficial vascular remodeling in limb ischemia is enhanced by exogenously administered proinflammatory chemokines such as monocyte-chemotactic protein-1 (MCP-1), 9 whereas remodeling is attenuated by monocyte depletion 10 or by functional inhibition of endothelial cell adhesion molecules or MCP-1 signaling. [11][12][13] Noninvasive imaging of key immune responses could potentially be used to study inflammation in vascular remodeling and how it can be modulated for therapeutic effect. Molecular imaging of inflammation with ultrasound has been achieved by surface modification of microbubble contrast agents.…”

Section: Clinical Perspective P 2911mentioning

confidence: 99%

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Molecular Imaging of Endothelial Vascular Cell Adhesion Molecule-1 Expression and Inflammatory Cell Recruitment During Vasculogenesis and Ischemia-Mediated Arteriogenesis

et al. 2008

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Background-Inflammatory responses contribute to vascular remodeling during tissue repair or ischemia. We hypothesized that inflammatory cell recruitment and endothelial cell activation during vasculogenesis and ischemia-mediated arteriogenesis could be temporally assessed by noninvasive molecular imaging. Methods and Results-Contrast ultrasound perfusion imaging and molecular imaging with microbubbles targeted to activated neutrophils, ␣ 5 -integrins, or vascular cell adhesion molecule (VCAM-1) were performed in murine models of vasculogenesis (subcutaneous matrigel) or hind-limb ischemia produced by arterial occlusion in wild-type or monocyte chemotactic protein-1-deficient mice. In subcutaneous matrigel plugs, perfusion advanced centripetally between days 3 and 10. On targeted imaging, signal enhancement from ␣ 5 -integrins and VCAM-1 coincided with the earliest appearance of regional blood flow. Targeted imaging correlated temporally with histological evidence of channel formation by ␣ 5 -integrinpositive monocytes, followed by the appearance of spindle-shaped cells lining the channels that expressed VCAM-1. In ischemic hind-limb tissue, skeletal muscle blood flow and arteriolar density increased progressively between days 2 and 21 after arterial ligation. Targeted imaging demonstrated early signal enhancement for neutrophils, monocyte ␣ 5 -integrin, and VCAM-1 at day 2 when blood flow was very low (Ͻ20% control). The neutrophil signal declined precipitously between days 2 and 4, whereas VCAM-1 and monocyte signal persisted to day 7. In mice deficient for monocyte chemotactic protein-1, monocyte-targeted signal was severely reduced compared with wild-type mice (

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

Cited by 52 publications

References 24 publications

Stretch-Induced Activation of the Transcription Factor Activator Protein-1 Controls Monocyte Chemoattractant Protein-1 Expression During Arteriogenesis

Stretch-Induced Activation of the Transcription Factor Activator Protein-1 Controls Monocyte Chemoattractant Protein-1 Expression During Arteriogenesis

The Role of Osteopontin in Recovery from Hind Limb Ischemia

Molecular Imaging of Endothelial Vascular Cell Adhesion Molecule-1 Expression and Inflammatory Cell Recruitment During Vasculogenesis and Ischemia-Mediated Arteriogenesis

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