Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
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.
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, http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-15136591, http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-15151905, http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-15269336, http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-16293605, http://linkedlifedata.com/resource/pubmed/commentcorrection/17371946-16322225, 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
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
110
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
519-28
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Mechanisms of induction of endothelial cell E-selectin expression by smooth muscle cells and its inhibition by shear stress.
pubmed:affiliation
Division of Medical Engineering Research, National Health Research Institutes, Miaoli, Taiwan, Republic of China. jjchiu@nhri.org.tw
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural