Transcriptome analysis of a population of control animals vs cisplatin-treated, in duplicate Overall design: A mixed population of worms representing all stages and growing under control conditions was exposed to 60 µg/ml of cisplatin for 24 hours at 20ºC. Treated and control samples weer collected in biological replicates.
Genetic and cellular sensitivity of <i>Caenorhabditis elegans</i> to the chemotherapeutic agent cisplatin.
Cell line, Treatment, SubjectView Samples
Microarray analysis was used to show that in gingival fibroblasts essentially all TGFB1 responsive genes were blocked by TAK inhibition
5Z-7-Oxozeanol Inhibits the Effects of TGFβ1 on Human Gingival Fibroblasts.
Specimen part, TreatmentView Samples
Development of spider veins is caused by the remodeling of veins located in the upper dermis and promoted by risk factors such as obesity or pregnancy that chronically increase venous pressure. We have repeatedly shown that the pressure-induced increase in biomechanical wall stress is sufficient to evoke the formation of enlarged corkscrew-like superficial veins in mice. Subsequent experimental approaches revealed that interference with endothelial- and/or smooth muscle cell activation counteracts this remodeling process. Here, we investigate whether the herbal agent glycyrrhetinic acid (GA) is a suitable candidate for that purpose given its anti-proliferative as well as anti-oxidative properties.
Glycyrrhetinic Acid Antagonizes Pressure-Induced Venous Remodeling in Mice.
Specimen part, SubjectView Samples
Although it is increasingly accepted that some paternal environmental conditions can influence phenotypes in future generations, it generally remains unclear whether the phenotypes induced in offspring represent specific responses to particular aspects of the paternal exposure history, or whether they represent a more generic response to paternal “quality of life”. To establish a paternal effect model based on a known ligand-receptor interaction and thereby enable pharmacological interrogation of the specificity of the offspring response, we explored the effects of paternal nicotine administration on offspring phenotype in mouse. We show that chronic paternal exposure to nicotine prior to reproduction induced a broad protective response to multiple xenobiotics in the next generation. This effect manifested as increased survival following an injection of toxic levels of either nicotine or of cocaine, was specific to male offspring, and was only observed after offspring were first acclimated to sublethal doses of nicotine or cocaine. Mechanistically, the reprogrammed state was characterized by enhanced clearance of nicotine in drug-acclimated animals, accompanied by hepatic upregulation of genes involved in xenobiotic metabolism. Surprisingly, this protective effect could also be induced by paternal exposure to a nicotinic receptor antagonist as well as to nicotine, suggesting that paternal xenobiotic exposure, rather than nicotinic receptor signaling, is likely to be responsible for programming of offspring drug resistance. Taken together, our data show that paternal drug exposure can induce a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics in the environment. Overall design: Hepatocytes were isolated from 8 week-old male F1 animals from control (TA) and nicotine-exposed (NIC) fathers, and allowed to adhere to the bottom of the well for three hours. Nonadherent cells were then removed, and fresh culture medium was then added. Cells were harvested at different time points in Trizol, and total RNA was extracted. Strand specific libraries were prepared from all samples, and sequenced on Illumina NextSeq500.
Paternal nicotine exposure alters hepatic xenobiotic metabolism in offspring.
Sex, Specimen part, Cell line, SubjectView Samples
The ability of dendritic cells (DCs) to activate immunity is linked to their maturation status. In prior studies we have shown that selective antibody-mediated blockade of inhibitory FcgRIIB receptor on human DCs in the presence of activating immunoglobulin (Ig) ligands leads to DC maturation and enhanced immunity to antibody-coated tumor cells. Here we show that Fcg receptor (FcgR) mediated activation of human monocytes and monocyte-derived DCs is associated with a distinct gene expression pattern, including several inflammation associated chemokines as well as type 1 interferon (IFN) response genes including the activation of signal transducer and activator of transcription 1 (STAT1).
Selective blockade of the inhibitory Fcgamma receptor (FcgammaRIIB) in human dendritic cells and monocytes induces a type I interferon response program.
No sample metadata fieldsView Samples
AFN-1252 is an inhibitor of fatty acid biosynthesis. Gene expression profiles were generated by microarray analysis of S. aureus cells following treatment with AFN-1252, an inhibitor of fatty acid synthesis.
Perturbation of Staphylococcus aureus gene expression by the enoyl-acyl carrier protein reductase inhibitor AFN-1252.
No sample metadata fieldsView Samples
We have examined the changes in gene expression aftert reatment of A549 cells, a cultured alveolar epithelial cells, with flagellin and transforming growth factor beta 1.
Induction of epithelial-mesenchymal transition by flagellin in cultured lung epithelial cells.
Specimen part, Cell lineView Samples
Oral squamous cell carcinoma (OSCC) is a prevalent form of cancer that develops from the epithelium of the oral cavity. OSCC is on the rise worldwide, and death rates associated with the disease are particularly high. Despite progress in understanding of the mutational and expression landscape associated with OSCC, advances in deciphering these alterations for the development of therapeutic strategies have been limited. Further insight into the molecular cues that contribute to OSCC is therefore required. Here we show that the transcriptional regulators YAP (YAP1) and TAZ (WWTR1), which are key effectors of the Hippo pathway, drive pro-tumorigenic signals in OSCC. Regions of pre-malignant oral tissues exhibit aberrant nuclear YAP accumulation, suggesting that dysregulated YAP activity contributes to the onset of OSCC. Supporting this premise, we determined that nuclear YAP and TAZ activity drives OSCC cell proliferation, survival, and migration in vitro, and is required for OSCC tumor growth and metastasis in vivo. Global gene expression profiles associated with YAP and TAZ knockdown revealed changes in the control of gene expression implicated in pro-tumorigenic signaling, including those required for cell cycle progression and survival. Notably, the transcriptional signature regulated by YAP and TAZ significantly correlates with gene expression changes occurring in human OSCCs identified by The Cancer Genome Atlas (TCGA), emphasizing a central role for YAP and TAZ in OSCC biology.
A YAP/TAZ-Regulated Molecular Signature Is Associated with Oral Squamous Cell Carcinoma.
Cell line, TreatmentView Samples
Nanoemulsion adjuvant affects immune gene expression in dendritic cells.
Distinct pathways of humoral and cellular immunity induced with the mucosal administration of a nanoemulsion adjuvant.
Specimen partView Samples
We investigated the molecular mechanisms for osteolytic bone metastasis by selecting human lung cancer cell line subpopulations with elevated metastatic activity and validating genes that are overexpressed in these cells. A bone-seeking squamous lung cancer cell line (HARA-B4) was established by sequentially injecting parental HARA cells into the left ventricle of male 5-week-old nude mice 4 times.
Involvement of CXCL14 in osteolytic bone metastasis from lung cancer.
Specimen part, Cell lineView Samples