Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6766
pubmed:dateCreated
2000-2-10
pubmed:abstractText
Atherosclerosis and post-transplant graft arteriosclerosis are both characterized by expansion of the arterial intima as a result of the infiltration of mononuclear leukocytes, the proliferation of vascular smooth muscle cells (VSMCs) and the accumulation of extracellular matrix. They are also associated with the presence of the immunomodulatory cytokine interferon-gamma (IFN-gamma). Moreover, in mouse models of atheroma formation or allogeneic transplantation, the serological neutralization or genetic absence of IFN-gamma markedly reduces the extent of intimal expansion. However, other studies have found that exogenous IFN-gamma inhibits cultured VSMC proliferation and matrix synthesis, and reduces intimal expansion in response to mechanical injury. This discrepancy is generally explained by the idea that IFN-gamma either directly activates macrophages, or, by increasing antigen presentation, indirectly activates T cells within the lesions of atherosclerosis and graft arteriosclerosis. These activated leukocytes are thought to express the VSMC-activating cytokines and cell-surface molecules that cause the observed arteriosclerotic responses. Here we have inserted pig and human arteries into the aorta of immunodeficient mice, and we show that IFN-gamma can induce arteriosclerotic changes in the absence of detectable immunocytes by acting on VSMCs to potentiate growth-factor-induced mitogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
13
pubmed:volume
403
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
207-11
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10646607-Adult, pubmed-meshheading:10646607-Animals, pubmed-meshheading:10646607-Arteriosclerosis, pubmed-meshheading:10646607-Cell Division, pubmed-meshheading:10646607-Cells, Cultured, pubmed-meshheading:10646607-Coronary Vessels, pubmed-meshheading:10646607-Histocompatibility Antigens, pubmed-meshheading:10646607-Humans, pubmed-meshheading:10646607-Image Processing, Computer-Assisted, pubmed-meshheading:10646607-Immunohistochemistry, pubmed-meshheading:10646607-Interferon-gamma, pubmed-meshheading:10646607-Leukocytes, pubmed-meshheading:10646607-Mice, pubmed-meshheading:10646607-Mice, SCID, pubmed-meshheading:10646607-Muscle, Smooth, Vascular, pubmed-meshheading:10646607-Platelet-Derived Growth Factor, pubmed-meshheading:10646607-Receptor, Platelet-Derived Growth Factor beta, pubmed-meshheading:10646607-Swine, pubmed-meshheading:10646607-Transplantation, Heterologous
pubmed:year
2000
pubmed:articleTitle
Interferon-gamma elicits arteriosclerosis in the absence of leukocytes.
pubmed:affiliation
Interdepartmental Program in Vascular Biology and Transplantation, Boyer Center for Molecular Medicine, and the Department of Surgery, Yale University School of Medicine, New Haven, Connecticut 06510, USA. george.tellides@yale.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't