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 journalArticlepeer-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 languageEnglish
Pages (from-to)936-942
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume310
Issue number3
DOIs
StatePublished - 24 Oct 2003

Keywords

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

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