CX3CR1 deficiency confers protection from intimal hyperplasia after arterial injury

Peng Liu, Sarita Patil, Mauricio Rojas, Alan M. Fong, Susan S. Smyth, Dhavalkumar D. Patel

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

OBJECTIVE - A functional polymorphism in the chemokine receptor CX3CR1 is associated with protection from vascular diseases including coronary artery disease and internal carotid artery occlusive disease. We investigated the mechanisms by which CX3CR1 may be involved by evaluating the inflammatory response to arterial injury in CX3CR1-deficient animals. METHODS AND RESULTS - Femoral arteries of CX3CR1 and wild-type (WT) mice were injured with an angioplasty guide wire. After 1, 5, 14, and 28 days, arteries were harvested and evaluated by histology, morphometry, and immunohistochemistry. Arterial injury upregulated the CX3CR1 ligand CX3CL1. In CX3CR1 compared with WT animals, the incidence of neointima formation was 58% lower (P=0.0017), accompanied by no difference in the area of platelet accumulation at day 1 (P=0.48) but a significant decrease in intimal monocyte infiltration at day 5 (P=0.006), vascular smooth muscle cell (VSMC) proliferation at days 5 and 14, and intimal area at day 28 (P=0.009). CONCLUSIONS - In an endothelial denudation injury model, CX3CR1 deficiency protects animals from developing intimal hyperplasia as a result of decreased monocyte trafficking to the lesion. CX3CR1 deficiency decreases VSMC proliferation and intimal accumulation either directly or indirectly as a result of defective monocyte infiltration.

Original languageEnglish
Pages (from-to)2056-2062
Number of pages7
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume26
Issue number9
DOIs
StatePublished - Sep 2006

Keywords

  • CX3CR1
  • Intimal hyperplasia
  • Monocytes
  • Smooth muscle cells
  • Vascular biology

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint

Dive into the research topics of 'CX3CR1 deficiency confers protection from intimal hyperplasia after arterial injury'. Together they form a unique fingerprint.

Cite this