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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0021753,
umls-concept:C0021755,
umls-concept:C0026809,
umls-concept:C0037083,
umls-concept:C0175630,
umls-concept:C0439792,
umls-concept:C0677535,
umls-concept:C1710082,
umls-concept:C1801960,
umls-concept:C2936381
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pubmed:issue |
4
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pubmed:dateCreated |
2006-3-27
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pubmed:abstractText |
Interleukin (IL)-1 is an important mediator of inflammation and cardiovascular disease. Here, we examined the role of IL-1 in arterial neointima formation. Carotid artery neointima was induced by ligation, and arteries were harvested 4 weeks after injury. The neointima/media of mice deficient in the IL-1 signaling receptor (IL-1R1(-/-)) was significantly reduced compared to IL-1R1(+/+) controls (P < 0.01). IL-1R1(+/+) mice receiving subcutaneous IL-1ra also had significantly reduced neointima/media compared with placebo (P < 0.05). IL-1beta(-/-) mice had reduced neointima/media compared to wild-type (P < 0.05), whereas IL-1alpha(-/-) mice were no different from controls. Mice deficient in the P2X(7) receptor (involved in IL-1 release) or caspase-1 (involved in IL-1 activation) did not differ in their response to carotid ligation compared to controls. To examine the site of IL-1 signaling, we generated chimeric mice. IL-1R1(+/+) mice receiving IL-1R1(-/-) marrow and IL-1R1(-/-) mice receiving IL-1R1(+/+) marrow both had significantly reduced neointima/media compared with IL-1R1(+/+) to IL-1R1(+/+) (P < 0.05) but had significantly greater neointima/media than IL-1R1(-/-) to IL-1R1(-/-) controls (P < 0.05). These data confirm the importance of IL-1beta signaling in mediating arterial neointima formation and suggest the involvement of IL-1 signaling in both circulating and arterial wall cells. Furthermore, receptor antagonism may be a better therapeutic target than interruption of IL-1beta processing or release.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-10339575,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-10615399,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-11015350,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-11016935,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-11073843,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-11316947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-11795265,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-11927948,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-12874179,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-1327576,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-15240711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-15254086,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-1574116,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-16099441,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-1919436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-2156847,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-2244864,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-2783498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-3047139,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-3052359,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-3288634,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-3485687,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-3519678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-7519205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-7544359,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-7722467,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-7859282,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-8609234,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-8840858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-8925587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-9015751,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-9029121,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-9233643,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-9317135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-9467064,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16565512-9565638
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0002-9440
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1396-403
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:16565512-Animals,
pubmed-meshheading:16565512-Carotid Artery, Common,
pubmed-meshheading:16565512-Carotid Stenosis,
pubmed-meshheading:16565512-Caspase 1,
pubmed-meshheading:16565512-Chimera,
pubmed-meshheading:16565512-Interleukin-1,
pubmed-meshheading:16565512-Mice,
pubmed-meshheading:16565512-Mice, Knockout,
pubmed-meshheading:16565512-Receptors, Interleukin-1,
pubmed-meshheading:16565512-Receptors, Purinergic P2,
pubmed-meshheading:16565512-Receptors, Purinergic P2X7,
pubmed-meshheading:16565512-Signal Transduction,
pubmed-meshheading:16565512-Tunica Intima
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pubmed:year |
2006
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pubmed:articleTitle |
Interleukin-1beta and signaling of interleukin-1 in vascular wall and circulating cells modulates the extent of neointima formation in mice.
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pubmed:affiliation |
Cardiovascular Research Unit, University of Sheffield, Clinical Sciences Centre, Northern General Hospital, Herries Road, Sheffield, S5 7AU, UK. j.chamberlain@sheffield.ac.uk
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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