Project description:Tumor Necrosis Factor-α is greatly implicated in heart pathophysiology, while it is upregulated in the failing myocardium. A major target in TNF-α-induced heart failure is the muscle specific intermediate filament cytoskeleton, comprised by desmin. We analysed the effect of cardiac-specific overexpression of TNF-α in the Des-/- myocardium, which is a known model of dilated cardiomyopathy. Hearts of 3 months old mice (n=3) of Des-/- and TNFαDes-/- genotypes were used for whole genome microarray hybridization analysis.
Project description:Tumor Necrosis Factor-α is greatly implicated in heart pathophysiology, while it is upregulated in the failing myocardium. A major target in TNF-α-induced heart failure is the muscle specific intermediate filament cytoskeleton, comprised by desmin. We analysed the effect of cardiac-specific overexpression of TNF-α in the Des-/- myocardium, which is a known model of dilated cardiomyopathy.
Project description:DES is a synthetic estrogen that is associated with adverse effects on reproductive organs. Our group has employed estrogen receptor (ER) α knockout (αERKO) mice to gain insight into the contribution of ER α in DES-induced toxicity following neonatal exposure
Project description:DES is a synthetic estrogen that is associated with adverse effects on reproductive organs. Our group has employed estrogen receptor (ER) α knockout (αERKO) mice to gain insight into the contribution of ER α in DES-induced toxicity following neonatal exposure
Project description:The pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-α), has been suggested to be a key factor in the induction of obesity-associated metabolic dysfunction. However, the role that macrophage-derived TNF-α has on regulating metabolic perturbations in obesity is not completely understood. Therefore, we utilized the TNF-αFlox/FLox (F/F), LyzMcre+/- mouse model to determine the impact that macrophage TNF-α deletion has on the development of high-fat-diet (HFD)-induced obesity.
Project description:DES is a synthetic estrogen that is associated with adverse effects on reproductive organs. Our group has employed estrogen receptor (ER) α knockout (αERKO) mice to gain insight into the contribution of ER a in DES-induced toxicity following neonatal exposure.
Project description:DES is a synthetic estrogen that is associated with adverse effects on reproductive organs. Our group has employed estrogen receptor (ER) α knockout (αERKO) mice to gain insight into the contribution of ER a in DES-induced toxicity following neonatal exposure.
Project description:DES is a synthetic estrogen that is associated with adverse effects on reproductive organs. Our group has employed estrogen receptor (ER) α knockout (αERKO) mice to gain insight into the contribution of ER-dependent pathways in mediating the effects of neonatal DES exposure in female and male reproductive tract tissues. The objective of this study is to compare gene expression profiles between the WT-veh and -DES groups or αERKO-veh and -DES from the adult male mice (week 10) of the SV tissues to identify differential genes.
Project description:Using a Cre-LoxP-based cell fusion assay we able to demonstrate that the fusion of human M13SV1-Cre breast epithelial cells and human MDA-MB-435-pFDR1 breast cancer cells was induced by TNF-alpha both under normoxic and hypoxic conditions. To investigate the impact of TNF-alpha on the gene expression profile of the cells M13SV1 and MDA-MB-435-pFDR1 cells were cultured for three days in the presence of 100ng/ml TNF-alpha both under normoxic and hypoxic conditions. Untreated cells served as a control. Subsequently, total RNA was extracted from the cells. Total RNA of three independent experiments that matched RIN criteria of 8 to 10 was pooled. Synthesis and Cy3 labeling of cDNA and hybridization of microarrays and microarray analysis was performed by Source Biosciences (Nottingham, UK). Microarray gene expression data were analyzed using GeneSpring GX v14.8 software (Agilent Technologies).
