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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-11-11
pubmed:abstractText
Thrombin acts as a potent mitogenic factor for ECs (endothelial cells) by the release of several growth factors, including PDGF-B (platelet-derived growth factor-B). CBP (CREB-binding protein), which functions as a transcriptional coactivator, links the changes in the extracellular stimuli with alterations in gene expression. Therefore, we hypothesized that CBP could mediate thrombin-induced proliferation of ECs via PDGF-B-dependent way. Short hairpin RNA was used to down-regulate the expression of CBP in ECs. CBP and PDGF-B levels were analysed by real-time RT-PCR and Western blot. To evaluate ECs proliferation, cell cycle and DNA synthesis were analysed by flow cytometry and BrdU (bromodeoxyuridine) incorporation assay, respectively. PDGF-B was involved in the mitogenic effect of thrombin on ECs. Down-regulation of CBP attenuated ECs proliferation and inhibited cell cycle progression induced by thrombin. Silencing CBP expression also suppressed thrombin-induced PDGF-B expression in ECs. Mitogenic activity of thrombin was impaired by silencing CBP expression in ECs. This inhibitory effect was, in part, related to the inability to up-regulate PDGF-B expression in ECs. CBP could be regarded as a potential therapeutic target for vascular injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1095-8355
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1155-61
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Down-regulation of CREB-binding protein expression inhibits thrombin-induced proliferation of endothelial cells: possible relevance to PDGF-B.
pubmed:affiliation
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, Peoples Republic of China. pyh_hongj@163.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't