Project description:We analyzed bone marrow derived neutrophils after they were left untreated, or treatment with LPS/IFNgamma (pro-inflammatory), IL4 (anti-inflammatory), insulin-like growth factor 1 and insulin to detect transcriptional changes after the different treatments.
Project description:1. evaluation of diagnostic importance of insulin like growth factor binding protein3 in patient with recently diagnosed as Colorectal cancer
2. correlation between the diagnostic efficacy of insulin like growth factor binding protein 3 with routine marker carcinoembryonic antigen.
Project description:Gastrodin alleviates cardiac hypertrophy by inhibition of insulin-like growth factor type 2/insulin-like growth factor type 2 receptor
Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Insulin-like growth factor 1 labeled with Cy5- time course with repeats Keywords: ordered
Project description:IGF1 and IGF1 receptors (IGF1R) are present in the adult heart and have been shown to be essential for myocardial performance. Insulin-like growth factor 1 (IGF1) is produced in numerous tissues particularly by the liver in response to growth hormone stimulation and is an important factor in the regulation of post-natal growth and development. We have generated and characterized transgenic mice over-expressing the IGF1R. We crossed IGF1R transgenic mice with dominant negative (dn)PI3K (p110) and with constitutively active (ca)PI3K(p110) transgenic mice. Expression profiling was performed on the ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age. Non-transgenic littermates were used as controls. Keywords = http://cardiogenomics.med.harvard.edu/groups/proj1/pages/igfr1_home.html Keywords: other
Project description:Research on the mechanism of Cytotoxic Necrotizing Factor 1 in regulating macrophage polarization.To study the molecular mechanisms through which CNF1 induces M1 macrophage polarization, we analyzed gene expression profiles of BMDMs treated with CNF1 or dialysis buffer.
Project description:Obesity-associated insulin resistance is characterized by a state of chronic, low-grade inflammation that is associated with the accumulation of M1 proinflammatory macrophages in adipose tissue. Although different evidence explains the mechanisms linking the expansion of adipose tissue and adipose tissue macrophage (ATM) polarization, in the current study we investigated the concept of lipid-induced toxicity as the pathogenic link that could explain the trigger of this response. We addressed this question using isolated ATMs and adipocytes from genetic and diet-induced murine models of obesity. Through transcriptomic and lipidomic analysis, we created a model integrating transcript and lipid species networks simultaneously occurring in adipocytes and ATMs and their reversibility by thiazolidinedione treatment. We show that polarization of ATMs is associated with lipid accumulation and the consequent formation of foam cell–like cells in adipose tissue. Our study reveals that early stages of adipose tissue expansion are characterized by M2-polarized ATMs and that progressive lipid accumulation within ATMs heralds the M1 polarization, a macrophage phenotype associated with severe obesity and insulin resistance. Furthermore, rosiglitazone treatment, which promotes redistribution of lipids toward adipocytes and extends the M2 ATM polarization state, prevents the lipid alterations associated with M1 ATM polarization. Our data indicate that the M1 ATM polarization in obesity might be a macrophage-specific manifestation of a more general lipotoxic pathogenic mechanism. This indicates that strategies to optimize fat deposition and repartitioning toward adipocytes might improve insulin sensitivity by preventing ATM lipotoxicity and M1 polarization. 15 samples; 2 genotypes and 2 time points
Project description:Insulin like growth factor binding protein-7 (IGFBP7) inhibits IGF signaling and functions as a potential tumor suppressor for hepatocellular carcinoma (HCC). We profiled genome-wide gene expression of Igfbp7 knockout (Igfbp7-/-) mouse to demonstrate the constitutive activation of IGF signaling and its relationship to the accelerated carcinogen-induced HCC.