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Down‐regulation of CREB‐binding protein expression inhibits thrombin‐induced proliferation of endothelial cells: possible relevance to PDGF‐B

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.