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 CynomolgusÂ MacaqueÂ Gene 1.0 STÂ Array.

2016-06-30 | E-GEOD-75759 | biostudies-arrayexpress

Macaca fascicularis

Project description:Formaldehyde and Epigenetic Alterations: MicroRNA Changes in the Nasal Epithelium of Nonhuman Primates

| PRJNA151111 | ENA

Identification of microRNA landscape of inflammation-induced colorectal carcinogenesis

Project description:Inflammatory conditions can contribute to tumor formation. However, any clear marker predicting progression to cancer are still lacking. The aim of our study was to analyze microRNA modulations accompanying inflammation-induced tumor development to determine whether these microRNA may jointly affect the expression of genes involved in cancer. For this purpose, we used the well-established azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model of colitis-associated cancer. We performed a microRNA microarray to establish microRNA expression profiles in mouse whole colon at early and late time points during inflammation and/or tumor growth. Chronic inflammation and carcinogenesis were associated with distinct changes in microRNA expression. Nevertheless, prediction algorithms of microRNA-mRNA interactions and computational analyses based on ranked microRNA lists consistently identified putative target genes that play essential roles in tumor growth or belong to key carcinogenesis-related networks or signaling pathways. Hence, inflammation, through microRNA, may affect unexpected genes or signaling pathways, thereby contributing to carcinogenesis. The present method can lead to the identification of novel genes or signaling pathways involved in cancer development.

2013-12-31 | GSE38443 | GEO

Formaldehyde-induced changes in microRNA signaling [Agilent]

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).

2014-01-07 | GSE42393 | GEO

Coordinated regulation of MAPK signaling pathway and microRNA in response to ionizing radiation in lung cancer cells

Project description:microRNA regulates cellular responses to ionizing radiation (IR) through the translational control of target genes. We analyzed time-series changes in microRNA expressions upon γ-irradiation in H1299 lung cancer cell lines using microarray. Significantly changed microRNAs were selected based on ANOVA analysis, target genes of which were enriched to MAPK signaling pathway. Concurrent analysis of mRNA and microRNA uncovered that the expression of miR-26b and its target ATF2 mRNA were inversely correlated in γ-irradiated H1299 cells. The overexpression of miR-26b induced the suppression of ATF2 in γ-irradiated cells. When we inhibit the MAPK signaling pathway using SP600125, JNK inhibitor, the expression of miR-26b was induced even in γ-irradiated H1299 cells. From these results, we concluded that the expression of miR-26b was coordinated regulated by MAPK signaling pathway upon ionizing radiation, and MAPK signaling pathway was regulated by miR-26b in turn.

2011-09-14 | GSE30075 | GEO

Global transcriptional response of Methylorubrum extorquens to formaldehyde stress includes both overlapping and unique gene sets in comparison to antibiotic translational inhibition and expands the role of EfgA

Project description:The potency and indiscriminate nature of formaldehyde reactivity upon biological molecules make it a universal stressor. However, some organisms such as Methylorubrum extorquens possess means to rapidly and effectively mitigate formaldehyde-induced damage. EfgA is a recently identified formaldehyde sensor predicted to halt translation in response to elevated formaldehyde as a means to protect cells. Herein, we investigate growth, formaldehyde consumption, and changes in gene expression to better understand how M. extorquens responds to formaldehyde with and without the EfgA-formaldehyde-mediated translational response, and how this mechanism compares to other forms of translation inhibition. These distinct mechanisms of translation inhibition have notable differences: they each involve different specific players and in addition, formaldehyde also acts as a general, multi-target stressor and a potential carbon source. Here, we present findings demonstrating that in addition to its characterized impact on translation, functional EfgA also allows for a rapid and robust transcriptional response to formaldehyde and that removal of efgA leads to heightened proteotoxic and genotoxic stress in the presence of increased formaldehyde levels. As our previous work suggested that formaldehyde is proteotoxic in M. extorquens, we accurately predicted that strains lacking efgA would experience increased protein damage. We also found that many downstream consequences of translation inhibition were shared by EfgA-formaldehyde- and kanamycin-mediated translation inhibition. Our work to modularize the transcriptional response uncovered additional layers of regulatory control enacted by functional EfgA upon experiencing formaldehyde stress, and further demonstrate the importance this protein plays at both transcriptional and translational levels in this model methylotroph.

2020-12-31 | GSE163955 | GEO

Rattus norvegicus

Project description:Gene Expression Changes in the Rat Nasal Epithelium Following Formaldehyde Exposure

| PRJNA99247 | ENA

Expression data from male cynomolgus macaques exposed to 6 ppm formaldehyde

2016-06-30 | GSE75759 | GEO