Gene expression profile of nickel-stimulated HUVEC
Ontology highlight
ABSTRACT: Nickel compounds, important carcinogens and prime inducers of contact allergy in humans, are potent activators of endothelial cells (ECs). To elucidate the signaling pathways mediating the cellular responses to nickel we performed Affymetrix gene profiling of human primary ECs. Keywords: stress response
Project description:We found that peripheral blood mononuclear cells (PBMCs) (from subjects with allergy to nickel) stimulated with nickel were characterized by a specific miRNA signature that were different from vehicle-stimulated PBMCs.
Project description:Our findings demonstrate that nickel-challenged skin in subjects with allergy to nickel is characterized by a specific miRNA signature compared to vehicle-challenged skin. In addition, we found that miRNA expression changes are different in allergic contact dermatitis (ACD to nickel) compared to irritant contact dermatitis (ICD).
Project description:Analysis of anti-CD3/anti-CD28 stimulated T cells treated with or without nickel chloride. Nickel is the most important contact allergen in the general population of the industrialized world. Results provide insight into the biological effects of nickel on human CD3+ T cells.
Project description:The goal of this study was to produce a reference transcriptome for the nickel hyperaccumulator Leucocroton havanensis endemic from Cuba and use this transcriptome as a reference to identify genes responding to the presence or the absence of nickel in both roots and shoots of this species
Project description:Nickel-resistant Saccharomyces cerevisiae mutant was obtained by evolutionary engineering. The reference strain which was used to select this nickel-resistant mutant could not grow even at 0.5 mM NiCl2 whereas this mutant was shown to be resistant upto 5.3 mM NiCl2 concentration. Whole-genome microarray analysis might be promising to identify the nickel resistance mechanisms in the yeast cells.
Project description:Nickel is an environmental toxicant prevalent in the atmosphere. Nickel exposure is associated with a multitude of human health hazards including chronic respiratory ailments and lung and nasal cancers. Our earlier studies on nickel exposure in lung cells showed that a majority of the gene expression changes caused by nickel exposure persisted even after termination of exposure (nickel-washed-out cells (NiW)). In this study, we wanted to examine the impact of a secondary toxicant exposure on the nickel-washed-out (NiW) cells as compared to the cells that were never exposed to nickel. To accomplish this, we exposed the untreated control cells (UT) and the nickel-washed-out cells (NiW) to multiple doses of nicotine (NTE). RNA-Seq analysis showed that the exposure of NiW cells to nicotine (NiW-NTE) caused unique gene expression changes that were markedly different from the gene expression changes caused by nicotine exposure of UT cells, which were never exposed to nickel. Analysis of the differentially expressed genes using Reactome Pathway analysis predicted interferon signaling only in the NiW-NTE cells. Upstream Regulator Analysis (URA) predicted STAT-1, a transcription factor that mediates cellular response to interferons, as the top potential upstream regulator in the NiW-NTE cells. Furthermore, chromatin immunoprecipitation (ChIP) analysis revealed increased STAT-1 binding at the promoters of genes associated with interferon signaling in NiW-NTE cells. Aberrant STAT-1 activation has been shown to promote carcinogenesis and interferon signaling promotes pathogenesis of autoimmune disease. Therefore, our results suggest that the epigenetic and transcriptional memory of the cells from the previous nickel exposure could negatively influence the outcome of secondary exposure to nicotine.
Project description:In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-α) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors. In order to identify potentially new soluble factors which greatly impact the self-renewal, proliferation and differentiation of CD34+ hematopoietic stem cells (HSC), we examined the expression profiles of IL-1ß, IL-3 and IL-6 stimulated human umbilical vein endothelial cells (HUVEC).
Project description:To gain further insights into a larger number of processes potentially altered by high nickel (Ni), we performed a transcriptional profiling of whole roots of Arabidopsis thaliana accession Columbia-0 (Col-0) exposed to 100 µM nickel, a concentration that induces slight chlorosis and intermediate inhibition of root and shoot growth.
Project description:Analysis of anti-CD3/anti-CD28 stimulated T cells treated with or without nickel chloride. Nickel is the most important contact allergen in the general population of the industrialized world. Results provide insight into the biological effects of nickel on human CD3+ T cells. We obtained mRNA of purified human CD3+ T cells from 3 different donors that were treated with or without 1000 μM nickel chloride for 1 h and then stimulated with anti-CD3/anti-CD28 for 6 h.