Raf Kinase Inhibitor Protein (RKIP) Inhibits Tumor Necrosis Factor-α (TNF-α) Induced Adhesion Molecules Expression in Vascular Smooth Muscle Bells by Suppressing (Nuclear Transcription Factor-κB (NF-kappaB) Pathway.

BACKGROUND Raf kinase inhibitor protein (RKIP) regulates growth and differentiation and plays a role in key signal transduction cascades in mammalian cells. Nevertheless, the underlying mechanism for which RKIP regulates cell-cell adhesion remains unknown. Our study investigated the function of the RKIP overexpression on adhesion molecules expression induced by tumor necrosis factor (TNF)-α in cultured mouse vascular smooth muscle cells (MOVACs). MATERIAL AND METHODS The expression levels of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were detected by ELISA kit, reverse transcription-PCR, and western blot assays. The protein expression of RKIP, p65, and inhibitor of nuclear factor (NF)-κBα (IκBα) were detected by western blot analysis. The activity of NF-kappaB was determined using a Dual-Luciferase Reporter assay. RESULTS The results showed that MOVACs transfected with pCMV5-HA-RKIP significantly inhibited TNF-α induced mRNA and protein expression of ICAM-1 and VCAM-1. The adhesion of THP-1 cells was also detected and inhibited by pCMV5-HA-RKIP in TNF-α-treated MOVACs. RKIP also suppressed the TNF-α-induced activation of NF-kappaB and the protein expression of phosphorylated IκB-α, and promoted the protein expression of IkB-α and nuclear translocation of p65 NF-kappaB. Furthermore, RKIP and the inhibitor of NF-kappaB (BAY11-7082) reduced the upregulation of ICAM-1 and VACM-1 induced by TNF-α. CONCLUSIONS Taken together, these results suggested that RKIP may inhibit the TNF-α-induced expression of adhesion molecules in MOVACs through inactivation of the NF-kappaB pathway.

[Combined use of optical coherence tomography and intravascular ultrasound during percutaneous coronary intervention in patients with coronary artery disease].

OBJECTIVE: To evaluate the value of combined optical coherence tomography (OCT) and intravascular ultrasound (IVUS) examinations in detecting coronary artery plaque during percutaneous transluminal coronary intervention (PCI). METHODS: OCT and IVUS examinations were performed on 30 diseased coronary vessels from 27 patients underwent PCI from Feb. 2008 to July. 2008. RESULTS: Seventeen vulnerable plaques (4 intima tearing which were not detected by IVUS), 5 plaque rupture (1 out of 5 was detected by IVUS), 5 thrombus lesions (1 out of 5 was found by IVUS), 12 thin-cap lipid-rich lesions (2 detected by IVUS) were detected by OCT in 22 lesions (without 8 lesions post DES stents). Analysis result of plaque burden by IVUS was superior to that obtained by OCT. In 8 DES stents (implanted for 6 months to 4 years), OCT detected 2 had severe restenosis, 6 stents struts were completely covered with neointima without restenosis, 1 stent had aneurysm-like dilatation. IVUS results were similar except for limitations on exactly detecting neointima post stenting. In 19 newly implanted stents, the incidence of stent under-expansion detected by OCT was 26.0% (same as that by IVUS), stent malposition was 63.2% (10.5% by IVUS, P < 0.01), near stent tearing was 10.5% (not detected by IVUS), tissue prolapse between coronary stent struts was 52.6% (10.5% in IVUS, P < 0.05). CONCLUSIONS: OCT imaging is superior to IVUS on detecting vulnerable plaques and change of structure around stents while IVUS is superior to OCT on estimating plaque burden in patients underwent PCI.