Project description:Percutaneous coronary intervention (PCI) with stent placement is a standard treatment for coronary artery disease (CAD). Despite all medical advances, restenosis remains a challenging clinical problem. However, the molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process and genetic predisposition is considered an important risk factor, analysis of the genome-wide gene expression is recommended for better insight of the phenomenon. We used microarray technology to monitor thousands of genes expression simultaneously. The whole genome expression will be analyzed with this technique to identify cluster of up-regulated and down-regulated genes which may be involved in this complex pathological condition. Coronary restenosis after percutaneous coronary intervention remains a challenging problem, despite all medical advances. Molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process. We used microarray technology to monitor thousands of genes expression simultaneously in restenosis postive group with reference restenosis negative group, which will unravel potentially modifiable pathways, possible targets and biomarkers for coronary restenosis.
Project description:Percutaneous coronary intervention (PCI) with stent placement is a standard treatment for coronary artery disease (CAD). Despite all medical advances, restenosis remains a challenging clinical problem. However, the molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process and genetic predisposition is considered an important risk factor, analysis of the genome-wide gene expression is recommended for better insight of the phenomenon. We used microarray technology to monitor thousands of genes expression simultaneously. The whole genome expression will be analyzed with this technique to identify cluster of up-regulated and down-regulated genes which may be involved in this complex pathological condition.
Project description:An unanticipated complication of the use of bare metal stents in percutaneous transluminal coronary angioplasty is in-stent restenosis resulting in >50% late lumen diameter loss in treated patients. In an effort to reduce in-stent restenosis, drug eluting stents containing the immunosuppressant sirolimus or zotarolimus have recently been developed. We report here the molecular response of arterial tissue to the implanting of these drug-eluting stents.
Project description:An unanticipated complication of the use of bare metal stents in percutaneous transluminal coronary angioplasty is in-stent restenosis resulting in >50% late lumen diameter loss in treated patients. In an effort to reduce in-stent restenosis, drug eluting stents containing the immunosuppressant sirolimus or zotarolimus have recently been developed. We report here the molecular response of arterial tissue to the implanting of these drug-eluting stents. Gene expression profiling was performed on 4 artery segments surrounding bare metal stents (BMS), 4 artery segments surrounding sirolimus-eluting stents (SES), and 4 artery segments surrounding zotarolimus-eluting stents (ZES) implanted into porcine animal models for 28 days.
Project description:To further development of our gene expression approach to cardiovascular disease, we have employed microarray expression profiling as a discovery platform to identify genes with the potential to distinguish the therapeutic target of the vein graft restenosis following coronary artery bypass grafting. Vein graft samples were obtained from model rats which received external jugular vein-carotid bypass grafting at different postoperative timepoints (n=3/group; day 7, 14 and 28, respectively). Vein samples were also obtained from control rats without vascular grafting (n=3/group; day 0). Time-dependent gene expression profiles were described with microarray analysis. Expression of three lncRNA-mRNA pairs (AF062402-Src, BC091437-Edg1 and BC166461- Mcam) from this signature were quantified in the same RNA samples by real-time PCR, confirming the accuracy of the microarray data.
Project description:Metals have been used for coronary artery stent materials in order to prevent stenosis caused by atherosclerosis. Degradable metallic materials (DMMs) are considered to be useful to avoid in-stent restenosis and late thrombosis. A new DMM, Fe-35Mn alloy, was fabricated through powder metallurgy in order to satisfy the ideal criteria of cardiovascular stent made of DMM. Since in-stent restenosis is mediated by the extracellular matrix production, which is mostly regulated by fibroblasts, the gene expression profile of 3T3 fibroblasts in the presence of Fe-35Mn alloy was then investigated. The mechanism of cellular responses in the presence of DMM is then expected to be clearly described through the gene profiling experiment.
Project description:Metals have been used for coronary artery stent materials in order to prevent stenosis caused by atherosclerosis. Degradable metallic materials (DMMs) are considered to be useful to avoid in-stent restenosis and late thrombosis. A new DMM, Fe-35Mn alloy, was fabricated through powder metallurgy in order to satisfy the ideal criteria of cardiovascular stent made of DMM. Since in-stent restenosis is mediated by the extracellular matrix production, which is mostly regulated by fibroblasts, the gene expression profile of 3T3 fibroblasts in the presence of Fe-35Mn alloy was then investigated. The mechanism of cellular responses in the presence of DMM is then expected to be clearly described through the gene profiling experiment. 3T3 fibroblast cells derived from mouse (Mus musculus) embryo (BALB/3T3 clone A31, ATTC) were put in the culture and treated with iron, manganese, and Fe-35Mn alloy for 24 hour in parallel and followed by the RNA extraction. Six technical replicates were included for treated cells as well as control cells.