Objective To determine the application values of gene chip technique in cardiovascular surgical clinical and research work. Microarray for gene expression profiles was used to screen out the differentially expressed genes during cardiopulmonary bypass(CPB) in peripheral blood mononuclear cell. By doing these, it was hoped that some clues in inflammatory response during CPB could be found out. Methods The patients’ oxygenated bloods were drawn immediately before onset and termination of CPB. Peripheral blood mononuclear cell (PBMC) were obtained from heparinised blood by Ficoll gradient centrifugation. The differentially expression was measured using BD AtlasTM cDNA Expression Arrays. The candidate genes were corroborated by semiquantitative reverse transcriptionpolymerase chain reaction (RT-PCR). Results Gene chip technique was successfully used in CPB study. The gene expression profiles of cytokines of PBMC during CPB were screened out. Interleukin 6 and Wnt5a were the differentially expressed genes. But the validity using semiquantitative RT-PCR found no statistically difference(P=0.888,0.135). Conclusion Microarray technique has positive application values in the study of cytokines during CPB. cDNA microarray for gene expression profiles can primarily screen out differentially expression genes during CPB. These genes may be engaged in inflammation and other pathophysiological reactions during CPB. PBMC is not the major source of cytokines during CPB.
Objective To determine the effect of insulin-like growth factor-1 (IGF-1) on angiogenesis in mouse breast cancer model of lower and normal serum IGF-1 levels after using angiogenesis inhibitor ginsenoside Rg3 （GS Rg3）. Methods The breast cancer models were established in control mice and liver specific IGF-1 deficient (LID) mice by feeding DMBA and were treated with GS Rg3. Vascular endothelial growth factor (VEGF) and F8-RAg were detected by immunohistochemical method in breast cancer tissues. IGF-1 gene and angiogenesis relating genes were detected by gene chip in breast cancer and normal breast tissue. Results The incidence rate of breast cancer in LID mice was lower than that in control mice (P＜0.05). VEGF expression and microvessel density of LID mice were lower than those in control mice (P＜0.05). Compared to the control mice, IGF-1, FGF-1, TGF-β1 and HGF genes were increased, and FGFR-2, PDGF-A and PDGF-B genes were decreased in breast cancer of LID mice. After GS Rg3 treatment, VEGFa, EGF, EGFR, PDGF-A and FGFR-2 genes were increased, IGF-1 and TGF-β1 genes were decreased in breast cancer of LID mice compared with the control mice. Conclusion IGF-1 may be involved in mouse breast cancer progression and associated with the growth of blood vessels. Angiogenesis inhibitor may play an antitumor role by IGF-1 and TGF-β1.
ObjectiveTo investigate the pathogenesis of atherosclerosis (AS) by detecting different expression genes between normal Wistar rats and rats with atherosclerosis through the technology of gene chip. MethodsThe rats were treated with standard diet with saline injection (control group) or high-cholesterol diet with vitamin D3 injection and balloon injury (model group). Total cholesterol (TC) and triglyeride (TG) in serum were detected 90 days later to ensure the success of establishment of the atherosclerosis model. Abdominal aorta was isolated and stained with HE. Total RNA was isolated from the aorta for gene chip analysis to explore the differential gene expression. ResultsCompared with the control group, the TC and TG level in the model group were highly advanced (P<0.05). AS model was confirmed by pathological observation. Gene chip detection showed that 511 genes were up-regulated and 1 219 ones were down-regulated which were interrelated with lipid metabolism, inflammatory reaction, oxidative stress and apoptosis as well. ConclusionThe expression change with multiple gene in AS suggests that the nosogenesis of AS is adjusted and controlled complicatedly. Intensive study of some important genes will contribute to the prevention and improvement of prognosis of AS.
ObjectiveTo investigate the significant genes in Mesio-temporal lobe epilepsy (MTLE) and explore the molecular mechanism of MTLE.MethodsThe microarray data of MTLE were downloaded from the Gene Expression Omnibus (GEO) database and analyzed by bioinformatics methods using GEO2R tool, Venny2.1.0, FUNRICH and Cytoscape software, DAVID and String databases.ResultsOf all the 331 differentially expressed genes(DEGs), 46 genes were down-regulated and 285 genes were up-regulated in dataset GSE88992; Furthermore, the core module genes were identified from those DEGs, which were expressed mostly in plasma membrane and extracellular space; The major molecular funtion were chemokine activity, cytokine activity and chemokine receptor binding; The main biological pathways involved neutrophil chemotaxis, inflammatory response and positive regulation of ERK1 and ERK2 cascade; The KEGG analysis showed DEGs enriched in Chemokine signaling pathway, Cytokine-cytokine receptor interaction and Complement and coagulation cascades. In addition, ten hub genes (Il6, Fos, Stat3, Ptgs2, Ccl2, Timp1, Cd44, Icam1, Atf3, Cxcl1) were found to significantly express in the MTLE.ConclusionThe pathogenesis of MTLE involves multiple genes, and multiple cell signaling pathways. Thus investigations of these genes may provide valuable insights into the mechanism of MTLE.