Pulmonary exposure to multiwalled carbon nanotubes (MWCNT) induces an inflammatory and rapid fibrotic response, although the long-term signaling mechanisms are unknown. The aim of this study was to examine the effects of 1, 10, 40, or 80 g MWCNT administered by pharyngeal aspiration on bronchoalveolar lavage (BAL) fluid for polymorphonuclear cell (PMN) infiltration, lactate dehydrogenase (LDH) activity, and lung histopathology for inflammatory and fibrotic responses in mouse lungs 1 mo, 6 mo, and 1 yr postexposure. Further, a 120-g crocidolite asbestos group was incorporated as a positive control for comparative purposes. Results showed that MWCNT increased BAL fluid LDH activity and PMN infiltration in a dose-dependent manner at all three postexposure times. Asbestos exposure elevated LDH activity at all 3 postexposure times and PMN infiltration at 1 mo and 6 mo postexposure. Pathological changes in the lung, the presence of MWCNT or asbestos, and fibrosis were noted at 40 and 80 g MWCNT and in asbestos-exposed mice at 1 yr postexposure. To determine potential signaling pathways involved with MWCNT-associated pathological changes in comparison to asbestos, up- and down-regulated gene expression was determined in lung tissue at 1 yr postexposure. Exposure to MWCNT tended to favor those pathways involved in immune responses, specifically T-cell responses, whereas exposure to asbestos tended to favor pathways involved in oxygen species production, electron transport, and cancer. Data indicate that MWCNT are biopersistent in the lung and induce inflammatory and fibrotic pathological alterations similar to those of crocidolite asbestos, but may reach these endpoints by different mechanisms.
Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study.
Specimen part
View SamplesThe STOX1 transcription factor has been involved in a complex human disease of pregnancy, preeclampsia, in human families, and mouse models. However, its mode of action is still largely unknown. Overexpression of either the long (STOX1A) or the short (STOX1B) isoform was obtained in the BeWo villous trophoblast model, a cell line able to fuse in syncytiotrophoblast following induction by forskolin treatment. The effects at the transcriptional level are evaluated in every condition.
Molecular Mechanisms of Trophoblast Dysfunction Mediated by Imbalance between STOX1 Isoforms.
Cell line, Treatment
View SamplesAnalysis of a SigX knockout mutant of Pseudomonas aeruginosa H103 strain in LB.
The absence of SigX results in impaired carbon metabolism and membrane fluidity in Pseudomonas aeruginosa.
No sample metadata fields
View SamplesA Single Cell Analysis of Myogenic Dedifferentiation Induced by Small Molecules An important direction in chemical biology is the derivation of compounds that affect cellular differentiation or its reversal. The fragmentation of multinucleate myofibers into viable mononucleates (called cellularisation) occurs during limb regeneration in urodele amphibians and the isolation of myoseverin, a tri-substituted purine that could apparently activate this pathway of myogenic dedifferentiation in mammalian cells, generated considerable interest. We have explored the mechanism and outcome of cellularisation at a single cell level, and report findings that significantly extend the previous work with myoseverin. Using a panel of compounds, including a novel triazine compound called 109 with structural similarity and comparable activity to myoseverin, we have identified microtubule disruption as critical for activation of the response. Our analysis has included the related control triazine compound 401, and the microtubule disrupting agent nocodazole. Time-lapse microscopy has enabled us to analyse the fate of identified mononucleate progeny, and directly assess the extent of dedifferentiation.
A single-cell analysis of myogenic dedifferentiation induced by small molecules.
Specimen part, Cell line, Compound, Time
View SamplesNaive spleens as well as naive and LPS-treated dendritic cells from wildtype and GPR34-/- mice were sequenced to integrate expression profiles with protein interaction networks and find functional modules that are affected by GPR34 Overall design: Expression profiles of dendritic cells and whole spleens were generated using Illumina HiSeq 2500/ Illumina HiScan
Dendritic Cells Regulate GPR34 through Mitogenic Signals and Undergo Apoptosis in Its Absence.
No sample metadata fields
View SamplesYears after the discovery that Dicer is a key enzyme in gene-silencing, the role of its helicase domain remains enigmatic. Here we show that this domain is critical for accumulation of certain endogenous small interfering RNAs (endo-siRNAs) in C. elegans. The domain is required for the production of the direct products of Dicer, or primary endo-siRNAs, and consequently, affects levels of downstream intermediates, the secondary endo-siRNAs. Consistent with the role of endo-siRNAs in silencing, their loss correlates with an increase in cognate mRNA levels. We find that the helicase domain of Dicer is not required for microRNA (miRNA) processing, or RNA interference following exposure to exogenous double-stranded RNA. Comparisons of wildtype and helicase-defective strains using deep-sequencing analyses show that the helicase domain is required by a subset of annotated endo-siRNAs, in particular, those associated with the slightly longer 26 nucleotide small RNA species containing a 5' guanosine. Overall design: We reintroduced either wildtype Dicer, or Dicer harboring a mutation (K39A) in it''s helicase domain, into dcr-1(ok247) mutant worms via transgene rescue. We then used high-throughput sequencing to compare levels of small RNAs present in each of these strains.
Dicer's helicase domain is required for accumulation of some, but not all, C. elegans endogenous siRNAs.
Cell line, Subject
View SamplesComparison of the changes in mitochondrial gene expression of cells in which extracellular growth factors and/or mitogens have been added.
Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis.
Specimen part
View SamplesWe describe here an interrupted reprogramming strategy to generate "induced Progenitor-Like (iPL) cells" from Alveolar Epithelial Type II (AEC-II) cells. A carefully defined period of transient expression of reprogramming factors (Oct4, Sox2, Klf4 and c-Myc; OSKM) is able to rescue the limited in vitro clonogenic capacity of AEC-II cells, potentially by activation of a bipotential progenitor-like state.
Interrupted reprogramming of alveolar type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis.
Specimen part
View SamplesWe obtained gene expression data and HD-SNP6.0 copy number data from PTL, PCNSL and PMLBCL samples and performed an integrative analysis on them. RNA was whole genome amplified using Nugen.
Targetable genetic features of primary testicular and primary central nervous system lymphomas.
Disease, Disease stage
View SamplesChickens divergently selected for either high growth (HG genotype) or low growth (LG genotype) at SRA-INRA, France were used to profile abdominal adipose gene expression at 7 wk of age. The HG and LG chickens are different in various phenotypic and metabolic measurements, including growth rate, abdominal fat, plasma glycemia, insulinemia, T4, T3, triglyceride and NEFA. The HG and LG chickens are valuable as a model for biomedical and agricultural traits. Massively parallel RNA sequencing (RNA-Seq) was completed on an Illumina HiSeq 2000 System for transcription analysis of HG and LG abdominal fat. Need information on data processing, statistical analysis, and differential expression. Keywords: abdominal fat, divergently selected chickens, growth, transcriptional profiling, differentially expressed genes Overall design: Abdominal fat mRNA profiles of high growth (HG genotype) or low growth (LG genotype) chickens at 7 weeks of age were generated by deep sequencing (on an Illumina HiSeq 2000 system).
Transcriptional analysis of abdominal fat in chickens divergently selected on bodyweight at two ages reveals novel mechanisms controlling adiposity: validating visceral adipose tissue as a dynamic endocrine and metabolic organ.
Age, Specimen part, Subject
View Samples