rdf:type |
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0115305,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0225336,
umls-concept:C0441712,
umls-concept:C1135918,
umls-concept:C1171318,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2007-7-3
|
pubmed:abstractText |
E-selectin is a major adhesion molecule expressed by endothelial cells (ECs), which are exposed to shear stress and neighboring smooth muscle cells (SMCs). We investigated the mechanisms underlying the modulation of EC E-selectin expression by SMCs and shear stress. SMC coculture induced rapid and sustained increases in expression of E-selectin and phosphorylation of interleukin-1 (IL-1) receptor-associated kinase glycoprotein-130, as well as the downstream mitogen-activated protein kinases (MAPKs) and Akt. By using specific inhibitors, dominant-negative mutants, and small interfering RNA, we demonstrated that activations of c-Jun-NH(2)-terminal kinase (JNK) and p38 of the MAPK pathways are critical for the coculture-induced E-selectin expression. Gel shifting and chromatin immunoprecipitation assays showed that SMC coculture increased the nuclear factor-kappaB (NF-kappaB)-promoter binding activity in ECs; inhibition of NF-kappaB activation by p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced E-selectin promoter activity. Protein arrays and blocking assays using neutralizing antibodies demonstrated that IL-1beta and IL-6 produced by EC/SMC cocultures are major contributors to the coculture induction of EC signaling and E-selectin expression. Preshearing of ECs at 12 dynes/cm(2) inhibited the coculture-induced EC signaling and E-selectin expression. Our findings have elucidated the molecular mechanisms underlying the SMC induction of EC E-selectin expression and the shear stress protection against this SMC induction.
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pubmed:grant |
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-10205148,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-11282896,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-12040186,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-12176889,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-12220554,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-12411390,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-12468429,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-12471242,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-14614942,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-14963004,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-15151905,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-15269336,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-16293605,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-16341264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-16466697,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-7535583,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-7544542,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-7632928,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-7943204,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-8521574,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-8572165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-9006914,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-9075932,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-9304801,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-9529157,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-9655393,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-9664085
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Jul
|
pubmed:issn |
0006-4971
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
110
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
519-28
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17371946-Animals,
pubmed-meshheading:17371946-Coculture Techniques,
pubmed-meshheading:17371946-E-Selectin,
pubmed-meshheading:17371946-Endothelium, Vascular,
pubmed-meshheading:17371946-Gene Expression Regulation,
pubmed-meshheading:17371946-Humans,
pubmed-meshheading:17371946-Interleukin-1,
pubmed-meshheading:17371946-Mice,
pubmed-meshheading:17371946-Mitogen-Activated Protein Kinases,
pubmed-meshheading:17371946-Muscle, Smooth, Vascular,
pubmed-meshheading:17371946-Signal Transduction,
pubmed-meshheading:17371946-Stress, Mechanical,
pubmed-meshheading:17371946-Umbilical Veins
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pubmed:year |
2007
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pubmed:articleTitle |
Mechanisms of induction of endothelial cell E-selectin expression by smooth muscle cells and its inhibition by shear stress.
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pubmed:affiliation |
Division of Medical Engineering Research, National Health Research Institutes, Miaoli, Taiwan, Republic of China. jjchiu@nhri.org.tw
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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