MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury

William J.H. Kim; Igor Chereshnev; Mihaela Gazdoiu; John T. Fallon; Barrett J. Rollins; Mark B. Taubman

doi:10.1016/j.bbrc.2003.09.088

MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury

William J.H. Kim, Igor Chereshnev, Mihaela Gazdoiu, John T. Fallon, Barrett J. Rollins, Mark B. Taubman

Research output: Contribution to journal › Article › peer-review

40 Scopus citations

Abstract

Monocyte chemoattractant protein (MCP)-1 is abundant in smooth muscle cells (SMC) and macrophages of atherosclerotic plaques and in the injured arterial wall. MCP-1 and its receptor, CCR2, are important mediators of macrophage accumulation and atherosclerotic plaque progression. We have recently reported that CCR2^-/- mice have a ≈60% decrease in intimal hyperplasia and medial DNA synthesis in response to femoral arterial injury. We have now examined the response to femoral arterial injury in MCP-1^-/- mice. MCP-1 deficiency was associated with a ≈30% reduction in intimal hyperplasia at 4 weeks and was not associated with diminished medial DNA synthesis. Despite inducing tissue factor in SMC culture, MCP-1 deficiency was not associated with a decrease in neointimal tissue factor after injury. These data suggest that MCP-1 and CCR2 deficiencies have distinct effects on arterial injury. The effects of MCP-1 on intimal hyperplasia may be mediated largely through SMC migration.

Original language	English
Pages (from-to)	936-942
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	310
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2003.09.088
State	Published - 24 Oct 2003

Keywords

Arterial injury
Chemokines
Intimal hyperplasia
Monocyte chemoattractant protein 1
Smooth muscle proliferation

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10.1016/j.bbrc.2003.09.088

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title = "MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury",

abstract = "Monocyte chemoattractant protein (MCP)-1 is abundant in smooth muscle cells (SMC) and macrophages of atherosclerotic plaques and in the injured arterial wall. MCP-1 and its receptor, CCR2, are important mediators of macrophage accumulation and atherosclerotic plaque progression. We have recently reported that CCR2-/- mice have a ≈60% decrease in intimal hyperplasia and medial DNA synthesis in response to femoral arterial injury. We have now examined the response to femoral arterial injury in MCP-1-/- mice. MCP-1 deficiency was associated with a ≈30% reduction in intimal hyperplasia at 4 weeks and was not associated with diminished medial DNA synthesis. Despite inducing tissue factor in SMC culture, MCP-1 deficiency was not associated with a decrease in neointimal tissue factor after injury. These data suggest that MCP-1 and CCR2 deficiencies have distinct effects on arterial injury. The effects of MCP-1 on intimal hyperplasia may be mediated largely through SMC migration.",

keywords = "Arterial injury, Chemokines, Intimal hyperplasia, Monocyte chemoattractant protein 1, Smooth muscle proliferation",

author = "Kim, {William J.H.} and Igor Chereshnev and Mihaela Gazdoiu and Fallon, {John T.} and Rollins, {Barrett J.} and Taubman, {Mark B.}",

note = "Funding Information: This work was supported in part by National Institutes of Health Grants HL29019 (M.B.T.) and HL61818 (M.B.T.).",

year = "2003",

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doi = "10.1016/j.bbrc.2003.09.088",

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AU - Kim, William J.H.

AU - Chereshnev, Igor

AU - Gazdoiu, Mihaela

AU - Fallon, John T.

AU - Rollins, Barrett J.

AU - Taubman, Mark B.

N1 - Funding Information: This work was supported in part by National Institutes of Health Grants HL29019 (M.B.T.) and HL61818 (M.B.T.).

PY - 2003/10/24

Y1 - 2003/10/24

N2 - Monocyte chemoattractant protein (MCP)-1 is abundant in smooth muscle cells (SMC) and macrophages of atherosclerotic plaques and in the injured arterial wall. MCP-1 and its receptor, CCR2, are important mediators of macrophage accumulation and atherosclerotic plaque progression. We have recently reported that CCR2-/- mice have a ≈60% decrease in intimal hyperplasia and medial DNA synthesis in response to femoral arterial injury. We have now examined the response to femoral arterial injury in MCP-1-/- mice. MCP-1 deficiency was associated with a ≈30% reduction in intimal hyperplasia at 4 weeks and was not associated with diminished medial DNA synthesis. Despite inducing tissue factor in SMC culture, MCP-1 deficiency was not associated with a decrease in neointimal tissue factor after injury. These data suggest that MCP-1 and CCR2 deficiencies have distinct effects on arterial injury. The effects of MCP-1 on intimal hyperplasia may be mediated largely through SMC migration.

AB - Monocyte chemoattractant protein (MCP)-1 is abundant in smooth muscle cells (SMC) and macrophages of atherosclerotic plaques and in the injured arterial wall. MCP-1 and its receptor, CCR2, are important mediators of macrophage accumulation and atherosclerotic plaque progression. We have recently reported that CCR2-/- mice have a ≈60% decrease in intimal hyperplasia and medial DNA synthesis in response to femoral arterial injury. We have now examined the response to femoral arterial injury in MCP-1-/- mice. MCP-1 deficiency was associated with a ≈30% reduction in intimal hyperplasia at 4 weeks and was not associated with diminished medial DNA synthesis. Despite inducing tissue factor in SMC culture, MCP-1 deficiency was not associated with a decrease in neointimal tissue factor after injury. These data suggest that MCP-1 and CCR2 deficiencies have distinct effects on arterial injury. The effects of MCP-1 on intimal hyperplasia may be mediated largely through SMC migration.

KW - Arterial injury

KW - Chemokines

KW - Intimal hyperplasia

KW - Monocyte chemoattractant protein 1

KW - Smooth muscle proliferation

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JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

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ER -

MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury

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Keywords

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