title: Ramping up RANTES in the acute response to arterial injury.
abstract: Arterial injury results in the formation of neointimal lesions. Lack of resolution of the pathologic neointima leads to stenosis, tissue ischemia, and organ dysfunction. In this issue of the JCI, Kovacic et al. show that, in response to arterial injury in mice, the cytokine TNF-alpha triggers a novel signaling pathway involving the combinatorial action of two transcription factors, STAT3 and NF-kappaB (p65 subunit), in VSMCs (see the related article beginning on page 303). Upon activation, these factors turn on transcription of a potent T cell chemokine, RANTES, which selectively recruits T cells into the vessel wall as part of the vascular wound-healing response.
authors.affiliation: Center for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10065, USA. tih2002@med.cornell.edu
authors.forename: Timothy
authors.initials: T
authors.lastname: Hla
authors.forename: Myat Lin
authors.initials: ML
authors.lastname: Oo
mesh_terms: D000818:Animals; D002465:Cell Movement; D018946:Chemokine CCL5 / Q000502:physiology*; D018925:Chemokines / Q000502:physiology; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000502:physiology; D051379:Mice; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D015398:Signal Transduction; D014652:Vascular Diseases / Q000378:metabolism*
chemical_list: C493957:Cdkn1a protein, mouse; D018946:Chemokine CCL5; D018925:Chemokines; D050759:Cyclin-Dependent Kinase Inhibitor p21