Expression data from male cynomolgus macaques exposed to 6 ppm formaldehyde
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ABSTRACT:
ORGANISM(S): Macaca mulatta Macaca fascicularis
PROVIDER: GSE75759 | GEO | 2016/06/30
SECONDARY ACCESSION(S): PRJNA305282
REPOSITORIES: GEO
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Project description:Exogenous formaldehyde disrupts genomic/epigenomic profiles in the rodent nose and white blood cells (WBCs) related to inflammation and immune signaling, although it does not reach the circulating blood. We aimed to compare and contrast alterations in genomic signaling in the nose and circulating blood of non-human primates exposed to formaldehyde. We used microarrays to identify transcripts that were diffentially expressed in response to formaldehyde inhalation exposure. A total of 14 primates received two consecutive days of 6-hour whole body inhalation exposures consisting of either filtered air (n = 6) or a target of 6 ppm formaldehyde (n = 8). To assess formaldehyde-induced changes in genome-wide gene expression profiles, RNA samples extracted from the nasal epithelium and circulating WBCs were labeled and hybridized to the Affymetrix Cynomolgus Macaque Gene 1.0 ST Array.
2016-06-30 | E-GEOD-75759 | biostudies-arrayexpress
Project description:In addition to gaining knowledge on in vivo miRNA responses to formaldehyde, we set out to relate these miRNA responses to transcriptional profiles modified by formaldehyde. Rats were exposed by inhalation to either 0 or 2 ppm formaldehyde (6 hours/day) for 28 days. Genome-wide transcriptional profiles and associated signaling pathways were assessed within the nasal respiratory mucosa and circulating mononuclear white blood cells (WBC). Male Fischer rats received nose-only inhalation exposures of 2 ppm formaldehyde for 7 days or 28 days (6 hours/day). Control (unexposed) rats were placed in nose-only exposure tubes containing room air for the same duration. After the last exposure period, animals were euthanized. RNA were assessed from sampes collected from the nasal epithelium and circulating white blood cells. Genome-wide mRNA expression profiles were evaluated using microarrays.
2014-01-07 | E-GEOD-42394 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) are critical regulators of gene expression, yet much remains unknown regarding miRNA changes resulting from environmental exposures and whether they influence pathway signaling across various tissues and time. To gain knowledge on these novel topics, we set out to investigate in vivo miRNA responses to inhaled formaldehyde, an important air pollutant known to disrupt miRNA expression profiles. Rats were exposed by inhalation to either 0 or 2 ppm formaldehyde (6 hours/day) for 7 days, 28 days, or 28 days followed by a 7 day recovery. Genome-wide miRNA expression profiles and associated signaling pathways were assessed within the nasal respiratory mucosa, circulating mononuclear white blood cells (WBC), and bone marrow (BM). Male Fischer rats received nose-only inhalation exposures of 2 ppm formaldehyde. Three exposure durations were investigated: (1) 2 ppm formaldehyde exposure, 6 hours/day, for 7 days (7-day group), (2) 2 ppm formaldehyde exposure, 6 hours/day, for 28 days (28-day group), and (3) 2 ppm formaldehyde exposure, 6 hours/day, for 28 days, with a 7 day recovery period following the last exposure (28-day plus recovery group). Control (unexposed) rats were placed in nose-only exposure tubes containing room air for the same duration. After the last exposure period (or the last recovery period for the 28-day plus recovery group), animals were euthanized. RNA were assessed from sampes collected from the nasal epithelium, circulating white blood cells, and bone marrow cells. Genome-wide miRNA expression profiles were evaluated using microarrays.
2014-01-07 | E-GEOD-42393 | biostudies-arrayexpress
Project description:In addition to gaining knowledge on in vivo miRNA responses to formaldehyde, we set out to relate these miRNA responses to transcriptional profiles modified by formaldehyde. Rats were exposed by inhalation to either 0 or 2 ppm formaldehyde (6 hours/day) for 28 days. Genome-wide transcriptional profiles and associated signaling pathways were assessed within the nasal respiratory mucosa and circulating mononuclear white blood cells (WBC).
2014-01-07 | GSE42394 | GEO
Project description:MicroRNAs (miRNAs) are critical regulators of gene expression, yet much remains unknown regarding miRNA changes resulting from environmental exposures and whether they influence pathway signaling across various tissues and time. To gain knowledge on these novel topics, we set out to investigate in vivo miRNA responses to inhaled formaldehyde, an important air pollutant known to disrupt miRNA expression profiles. Rats were exposed by inhalation to either 0 or 2 ppm formaldehyde (6 hours/day) for 7 days, 28 days, or 28 days followed by a 7 day recovery. Genome-wide miRNA expression profiles and associated signaling pathways were assessed within the nasal respiratory mucosa, circulating mononuclear white blood cells (WBC), and bone marrow (BM).
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Project description:Circulating tumor cells (CTCs) are precursors of metastasis in several cancer types, and are occasionally found within the bloodstream in association with non-malignant cells such as white blood cells (WBCs). The identity and function of these CTC-associated WBCs, as well as the molecular features that define the interaction between WBCs and CTCs are unknown. Here, we achieve the isolation and interrogation of individual CTC-associated WBCs, alongside with corresponding cancer cells within each CTC-WBC-cluster, from multiple breast cancer patients and mouse models.
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Project description:Formaldehyde (FA), an endogenous cellular aldehyde, is a rat nasal carcinogen. In this study, concentration- and exposure-duration transitions in FA mode of action (MOA) were examined with pharmacokinetic (PK) modeling for tissue formaldehyde acetal (FAcetal) and glutathione (GSH) and with histopathology and gene expression studies for tissue responses in nasal epithelium from rats exposed to 0, 0.7, 2, 6, 10 or 15 ppm FA 6 hr/day for 1, 4 or 13 weeks. The study had two goals. The first goal was to develop a basic PK model to estimate various forms of tissue formaldehyde and tissue glutathione (GSH). The second goal was to compare histopathology and gene expression changes in nasal tissues caused by inhalation of FA with changes in tissue FAcetal and free GSH calculated from the PK model. Patterns of gene expression varied with concentration and with duration. At 0.7 and 2 ppm, sensitive response genes (SRGs) - associated with cellular stress, thiol transport/reduction, inflammation, and cell proliferation - were similarly upregulated at all exposure durations. At 6 ppm and greater, gene expression changes showed enrichment of pathways involved in cell cycle, DNA repair, and apoptosis processes. ERBB, EGFR, WNT, TGF-β, Hedgehog, and Notch signaling were also enriched in differentially expressed genes. Benchmark doses (BMDs) for genes in significantly enriched pathways were lower at 13 weeks than at 1 or 4-week. The transcriptional and histological changes corresponded to PK model-predicted changes in free GSH at 0.7 and 2 ppm and in FAcetal at 6 ppm. DNA-replication stress, enhanced proliferation, metaplasia, and stem cell-niche activation appear to be associated with FA carcinogenesis at 6 ppm and above. Dose dependencies in MOA, the presence of high physiological FAcetal, and non-linear FAcetal/GSH tissue kinetics indicate that FA concentrations below 150 ppb (and probably any concentrations below irritant levels, i.e., ~ 1 ppm) would not increase cancer risks of inhaled FA in the nose or any other tissue. Closer examination of dose response relationships for endogenous compound toxicity could help guide biologically relevant approaches for chemical risk assessment. Eight week old male F344/CrlBR rats were exposed to formaldehyde through whole body inhalation. Whole-body exposures were performed at doses of 0, 0.7, 2, 6, 10, and 15 ppm (6 hours per day, 5 days per week). Inhalation animals were sacrified at 1, 4, and 13 weeks following initiation of exposure. Following sacrifice, tissue from the Level II region of the nose was dissected and digested with a mixture of proteases to remove the epithelial cells. The epithelial cells acquired from this section of the nose consisted primarily of transitional epithelium with some respiratory epithelium. Gene expression microarray analysis was performed on the epithelial cells.
2010-07-28 | E-GEOD-23179 | biostudies-arrayexpress
Project description:Formaldehyde is a toxic volatile organic compound and its mechanism of toxicity to plant has not yet been revealed. This experiment was designed to identify formaldehyde-responsible genes under exposure to low or high concentration of airborne formaldehyde for a short period of time. 7 weeks old Arabidopsis thaliana transformant (ecotype: Columbia) plants were exposed to gaseous formaldehyde at 1-2 ppm (low), 14-16 ppm (high), or less than 0.04 ppm (air control) at 24oC under light-condition for 150 minutes inside a chamber for formaldehyde exposure. Total RNA was isolated from rosette leaves of exposed plants and was applied to microarray analysis. We investigated into formaldehyde dose response on gene expression of Arabidopsis and tried to understand the toxic mechanisms of formaldehyde using an Affymetrix Arabidopsis genome array ATH-1.
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Project description:In order for bacteria to thrive, they must be well-adapted to their environmental niche, which may involve specialized metabolism, timely adaptation to shifting environments, and/or the ability to mitigate numerous stressors. These attributes are highly dependent on cellular machinery that can sense both the external and intracellular environment. Methylorubrum extorquens is an extensively studied facultative methylotroph, an organism that can use single-carbon compounds as their sole source of carbon and energy. In methylotrophic metabolism, carbon flows through formaldehyde as a central metabolite; thus, formaldehyde is both an obligate metabolite and a metabolic stressor. Via the one-carbon dissimilation pathway, free formaldehyde is rapidly incorporated by formaldehyde activating enzyme (Fae), which is constitutively expressed at high levels. In the presence of elevated formaldehyde levels, a recently identified formaldehyde-sensing protein, EfgA, induces growth arrest. Herein, we describe TtmR, a formaldehyde-responsive transcription factor that, like EfgA, modulates formaldehyde resistance. It is a member of the MarR family of transcription factors and impacts the expression of 75 genes distributed throughout the genome, many of which are themselves transcription factors and/or involved in stress response, including efgA. Notably, when M. extorquens is adapting its metabolic network during the transition to methylotrophy, efgA and ttmR mutants experience an imbalance in formaldehyde production and a notable growth delay. Although methylotrophy necessitates that M. extorquens maintain a relatively high level of formaldehyde tolerance, this work reveals a tradeoff between formaldehyde resistance and the efficient transition to methylotrophic growth and suggests that TtmR and EfgA play a pivotal role in maintaining this balance.
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