title: Differential endothelial coverage, response to injury and neointimal integration of CX3CR1/smooth muscle-like cells after carotid or femoral arterial injury.
abstract: BACKGROUND
  Previously, we established the importance of the CX3CL1/CX3CR1 axis in the promotion of myeloid cell differentiation into neointimal smooth muscle-like cells (SMLC).
  
  
  METHODS
  In this study, acute (24 h) endothelial coverage and CX3CL1 expression as well as chronic (2 weeks) vascular remodeling was examined with respect to whether myeloid CX3CR1(+) SMLC number in the neointima differed between carotid and femoral artery wire injury.
  
  
  CONCLUSIONS
  Twenty-four hours after injury, CX3CL1 expression was significantly elevated in injured carotid compared to femoral arteries. In mice with CX3CR1 promoter-driven expression of green fluorescent protein, neointima formation was significantly greater (p < 0.05) 2 weeks after injury in femoral versus carotid arteries as determined by the intima/media ratio. Although the percentage of F4/80/CX3CR1(+) cell integration was similar in both models, the carotid lesion had greater proportions of cells coexpressing CX3CR1 and both α-smooth muscle actin and calponin (p < 0.05). Wire injury of carotid arteries was associated with greater CX3CL1 expression in the acute phase followed by greater CX3CR1 coexpressing SMLC content in later lesions as well as less neointima formation than in femoral arteries. This may, in part, explain the variability in lesion composition after carotid versus femoral wire injury.
authors: Biosciences Institute, University College Cork, Centre for Research in Vascular Biology, Cork, Ireland.
authors: Kenneth
authors: K
authors: Martin
authors: Arun H S
authors: AH
authors: Kumar
authors: Kerstin
authors: K
authors: Klinkert
authors: Noel M
authors: NM
authors: Caplice
mesh_terms: D000199:Actins / Q000235:genetics; D000210:Acute-Phase Reaction; D000818:Animals; D001792:Blood Platelets / Q000473:pathology; D000073883:CX3C Chemokine Receptor 1; D002135:Calcium-Binding Proteins / Q000235:genetics; D002339:Carotid Arteries / Q000737:chemistry / Q000473:pathology; D020212:Carotid Artery Injuries / Q000473:pathology / Q000503:physiopathology*; D054428:Chemokine CX3CL1 / Q000032:analysis / Q000235:genetics / Q000502:physiology; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology*; D005263:Femoral Artery / Q000737:chemistry / Q000293:injuries* / Q000473:pathology; D015870:Gene Expression; D049452:Green Fluorescent Proteins / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008840:Microfilament Proteins / Q000235:genetics; D018613:Microscopy, Confocal; D032389:Myocytes, Smooth Muscle / Q000502:physiology*; D058426:Neointima / Q000503:physiopathology*; D009504:Neutrophils / Q000473:pathology; D011401:Promoter Regions, Genetic / Q000235:genetics; D019707:Receptors, Chemokine / Q000502:physiology*; D000096985:Calponins
chemical_list: D000199:Actins; D000073883:CX3C Chemokine Receptor 1; D002135:Calcium-Binding Proteins; D054428:Chemokine CX3CL1; D049452:Green Fluorescent Proteins; D008840:Microfilament Proteins; D019707:Receptors, Chemokine; D000096985:Calponins; C471885:Cx3cr1 protein, mouse; C544013:alpha-smooth muscle actin, mouse