Source:http://linkedlifedata.com/resource/pubmed/id/15982660
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-1-9
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pubmed:abstractText |
The cysteine protease cathepsin L is one of the most potent mammalian elastases and collagenases, widely expressed at basal levels in most tested tissues and cell types, and regulated by pro-inflammatory stimuli. The inflammatory arterial diseases abdominal aortic aneurysm (AAA) and atherosclerosis involve extensive vascular remodeling that requires elastolysis and collagenolysis. This study examined the hypothesis that cathepsin L is over-expressed in human AAA and atherosclerotic lesions and its expression in vascular cell types found in these lesions is regulated by pro-inflammatory cytokines. Immunohistochemical and tissue extract immunoblot analysis demonstrated increased expression of cathepsin L in human AAA and atheromata and localized its expression to lesional smooth muscle cells (SMC), endothelial cells (EC), and macrophages. In primary cultured human SMC, EC, and monocyte-derived macrophages, pro-inflammatory cytokines or growth factors induced the expression of cathepsin L and its activity against extracellular collagen and elastin. Patients with coronary artery stenosis (n=65) had higher serum cathepsin L levels than those without lesions detectable by quantitative coronary angiography (n=30) (1.47+/-0.33 ng/ml versus 0.60+/-0.06 ng/ml, p<0.02). A strong correlation between the percent of stenosis of left anterior descending coronary artery and serum cathepsin L levels in patients with stenosis (R=0.542, p<0.0001), also suggests involvement of cathepsin L in these vascular diseases.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CTSL1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cathepsin L,
http://linkedlifedata.com/resource/pubmed/chemical/Cathepsins,
http://linkedlifedata.com/resource/pubmed/chemical/Ctsl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9150
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pubmed:author |
pubmed-author:DolganovGregory MGM,
pubmed-author:FuHuanxiangH,
pubmed-author:HuChengchengC,
pubmed-author:LibbyPeterP,
pubmed-author:LiuJianJ,
pubmed-author:MaLikunL,
pubmed-author:ShiGuo-PingGP,
pubmed-author:SukhovaGalina KGK,
pubmed-author:SunJiusongJ,
pubmed-author:TioLL,
pubmed-author:XuWei-HuaWH,
pubmed-author:YangJin-TianJT
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pubmed:issnType |
Print
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pubmed:volume |
184
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
302-11
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15982660-Animals,
pubmed-meshheading:15982660-Aortic Aneurysm, Abdominal,
pubmed-meshheading:15982660-Atherosclerosis,
pubmed-meshheading:15982660-Cathepsin L,
pubmed-meshheading:15982660-Cathepsins,
pubmed-meshheading:15982660-Cells, Cultured,
pubmed-meshheading:15982660-Cysteine Endopeptidases,
pubmed-meshheading:15982660-Endothelium, Vascular,
pubmed-meshheading:15982660-Enzyme Precursors,
pubmed-meshheading:15982660-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:15982660-Gene Expression Regulation,
pubmed-meshheading:15982660-Humans,
pubmed-meshheading:15982660-Macrophages, Peritoneal,
pubmed-meshheading:15982660-Mice,
pubmed-meshheading:15982660-Muscle, Smooth, Vascular,
pubmed-meshheading:15982660-Polymerase Chain Reaction,
pubmed-meshheading:15982660-RNA, Messenger,
pubmed-meshheading:15982660-Saphenous Vein
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pubmed:year |
2006
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pubmed:articleTitle |
Cathepsin L expression and regulation in human abdominal aortic aneurysm, atherosclerosis, and vascular cells.
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pubmed:affiliation |
Department of Cell and Molecular Biology, University of Science and Technology of China, Hefei, China.
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pubmed:publicationType |
Journal Article,
Comparative Study,
In Vitro,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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