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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1998-8-26
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pubmed:abstractText |
Formation of the atherosclerotic intima must involve altered metabolism of the elastin-rich arterial extracellular matrix. Proteases potentially involved in these processes remain unclear. This study examined the expression of the potent elastases cathepsins S and K in human atheroma. Normal arteries contained little or no cathepsin K or S. In contrast, macrophages in atheroma contained abundant immunoreactive cathepsins K and S. Intimal smooth muscle cells (SMC), especially cells appearing to traverse the internal elastic laminae, also contained these enzymes. Extracts of atheromatous tissues had approximately twofold greater elastase-specific activity than extracts of uninvolved arteries, mostly due to cysteine proteases. Cultured human SMC displayed no immunoreactive cathepsins K and S and exhibited little or no elastolytic activity when incubated with insoluble elastin. SMC stimulated with the atheroma-associated cytokines IL-1beta or IFN-gamma secreted active cathepsin S and degraded substantial insoluble elastin (15-20 microg/10(6) cells/24 h). A selective inhibitor of cathepsin S blocked > 80% of this elastolytic activity. The presence of cathepsins K and S at sites of vascular matrix remodeling and the ability of SMC and macrophages to use these enzymes to degrade elastin supports a role for elastolytic cathepsins in vessel wall remodeling and identifies novel therapeutic targets in regulating plaque stability.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-1281481,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-1373132,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-1444473,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-1896464,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-1918003,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-2012168,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-2176623,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-2508645,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-3306285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-3491091,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-6302107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-6556916,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-7005386,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-7615167,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-7634481,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-7731994,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-7805878,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-7989608,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8083356,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8157683,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8281670,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8444861,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8507218,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8567669,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8612130,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8647859,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8647860,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8703060,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-8873680,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-9143504,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-9151110,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-9393764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9691094-9560298
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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 |
Aug
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pubmed:issn |
0021-9738
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
102
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
576-83
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:9691094-Arteriosclerosis,
pubmed-meshheading:9691094-Carotid Stenosis,
pubmed-meshheading:9691094-Cathepsin K,
pubmed-meshheading:9691094-Cathepsins,
pubmed-meshheading:9691094-Cells, Cultured,
pubmed-meshheading:9691094-Coronary Disease,
pubmed-meshheading:9691094-Elastin,
pubmed-meshheading:9691094-Enzyme Induction,
pubmed-meshheading:9691094-Humans,
pubmed-meshheading:9691094-Interferon-gamma,
pubmed-meshheading:9691094-Muscle, Smooth, Vascular,
pubmed-meshheading:9691094-RNA, Messenger,
pubmed-meshheading:9691094-Tunica Intima
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pubmed:year |
1998
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pubmed:articleTitle |
Expression of the elastolytic cathepsins S and K in human atheroma and regulation of their production in smooth muscle cells.
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pubmed:affiliation |
Brigham and Women's Hospital, Vascular Medicine and Atherosclerosis Unit and Cardiovascular and Respiratory Divisions, Department of Medicine, Boston, Massachusetts 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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