| Insulin-like growth factor-I receptors in atherosclerotic plaques of symptomatic and asymptomatic patients with carotid stenosis: effect of IL-12 and IFN-gamma. | |
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MedLine Citation:
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PMID: 17040964 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The balance between apoptosis and survival of vascular smooth muscle cells (VSMCs) in the fibrous cap appears to best correlate with plaque instability or stability and is controlled by growth factors and cytokines. We recently reported the inhibition of insulin-like growth factor (IGF)-I-induced proliferation and increase in apoptosis of VSMCs by atheroma-associated cytokines. Here we assessed the expression of IGF-I receptor (IGF-IR) in atherosclerotic plaques and in plaque VSMCs of asymptomatic and symptomatic patients with carotid stenosis and examined the effect of IGF-I, IL-12, and IFN-gamma on the expression of IGF-IR and IGF-binding protein (IGFBP)-3 in plaque VSMCs. We observed significantly lower density of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive apoptotic nuclei and increased positive immunoreactivity to IGF-IR and mRNA transcripts of endogenous IGF-I and IGF-IR in asymptomatic than in symptomatic plaque VSMCs. Positive correlation was found between apoptosis and IGF-IR expression in asymptomatic (r(2) = 0.942) and symptomatic (r(2) = 0.908) plaque VSMCs. The specific binding of (125)I-labeled IGF-I was 3.7-fold higher in plaque VSMCs of asymptomatic patients than in symptomatic patients. IGF-I increased both IGF-IR mRNA transcripts and expression of IGFBP-3 in VSMCs of asymptomatic plaques. IL-12 and IFN-gamma decreased IGF-IR mRNA transcripts and further increased the expression of IGFBP-3 in asymptomatic VSMCs but had no effect in symptomatic VSMCs. These data suggest that the decreased expression of IGF-IR mRNA and increased expression of IGFBP-3 in carotid plaques of symptomatic patients could be due to atheroma-associated cytokines and this could result in plaque instability. |
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Authors:
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Guanghong Jia; Gang Cheng; Krish Soundararajan; Devendra K Agrawal |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural Date: 2006-10-13 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 292 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2007 Feb |
Date Detail:
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Created Date: 2007-02-08 Completed Date: 2007-03-20 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1051-7 Citation Subset: IM |
Affiliation:
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Department of Biomedical Science, Creighton University School of Medicine, Omaha, Nebraska 68178, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Apoptosis Carotid Artery Diseases / complications, metabolism*, pathology Carotid Stenosis / etiology, physiopathology*, surgery Cells, Cultured Endarterectomy, Carotid Female Humans Immunohistochemistry In Situ Nick-End Labeling Insulin-Like Growth Factor Binding Proteins / metabolism* Insulin-Like Growth Factor I / metabolism Interferon-gamma / metabolism*, pharmacology Interleukin-12 / metabolism*, pharmacology Male Muscle, Smooth, Vascular / metabolism Myocytes, Smooth Muscle / metabolism RNA, Messenger / metabolism Receptor, IGF Type 1 / metabolism* Reverse Transcriptase Polymerase Chain Reaction |
| Grant Support | |
ID/Acronym/Agency:
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R01-HL-070885/HL/NHLBI NIH HHS; R01-HL-073349/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/IGFBP3 protein, human; 0/Insulin-Like Growth Factor Binding Proteins; 0/RNA, Messenger; 187348-17-0/Interleukin-12; 67763-96-6/Insulin-Like Growth Factor I; 82115-62-6/Interferon-gamma; EC 2.7.10.1/Receptor, IGF Type 1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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