RNA-seq of cells in Mus musculus nasal turbinates with or without 7DW8-5 treatment
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina HiSeq 4000
ORGANISM(S): Mus musculus
SUBMITTER: Kazuya Masuda
PROVIDER: E-MTAB-12345 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We performed proteomic analyses of human olfactory epithelial tissue to identify missing proteins using liquid chromatography-tandem mass spectrometry. Using a next-generation proteomic pipeline with a <1.0% false discovery rate at the peptide and protein levels, we identified 3,731 proteins, among which five were missing proteins (P0C7M7, P46721, P59826, Q658L1, and Q8N434). We validated the identified missing proteins using the corresponding synthetic peptides. We also identified 49 and 50 alternative splicing variants mapped at the neXtProt and GENCODE databases, respectively, and 2,000 additional single amino acid variants.
2018-08-17 | PXD010025 | Pride
Project description:We investigated the effects of PACAP treatment, and endogenous PACAP deficiency, on infarct volume, neurological function, and the cerebrocortical transcriptional response in a mouse model of stroke, middle cerebral artery occlusion (MCAO). PACAP-38 administered i.v. or i.c.v. one hour after MCAO significantly reduced infarct volume, and ameliorated functional motor deficits measured 24 hours later in wild-type mice. Infarct volumes and neurological deficits (walking faults) were both greater in PACAP-deficient than in wild-type mice, but treatment with PACAP reduced lesion volume and neurological deficits in PACAP-deficient mice to the same level of improvement as in wild-type mice. A 35,546-clone mouse cDNA microarray was used to investigate cortical transcriptional changes associated with cerebral ischemia in wild-type and PACAP-deficient mice, and with PACAP treatment after MCAO in wild-type mice. 229 known (named) transcripts were increased (228) or decreased (1) in abundance at least 50% following cerebral ischemia in wild-type mice. 49 transcripts were significantly up-regulated only at one hour post-MCAO (acute response transcripts), 142 were up-regulated only at 24 hours post-MCAO (delayed response transcripts) and 37 transcripts were up-regulated at both times (sustained response transcripts). More than 50% of these are transcripts not previously reported to be associated with brain ischemia responses. Many of the acutely regulated neurotrauma-associated transcripts, but a larger percentage of the delayed ones, require endogenous PACAP for up-regulation by ischemia, suggesting a more prominent role for PACAP in later response to injury than in the initial response, and consistent with a neuroprotective role for PACAP in late response to injury and neuroprotective efficacy when given post-MCAO. Putative injury effector transcripts regulated by PACAP include ãÃ-actin, midline 2, and metallothionein 1. Potential neuroprotective transcripts include several demonstrated to be PACAP-regulated in other contexts. Prominent among these were transcripts encoding the PACAP-regulated gene Ier3, and the neuropeptides enkephalin, substance P (tachykinin 1), and neurotensin. In the hybridization method employed, equal amounts (2-5ãÃg/15.5 ãÃl) of total RNA obtained from brain tissue of different experimental groups were separately labeled with two different fluorescent dyes (Cy3 or Cy5) and applied on the same NIMH Mouse 36K cDNA microarray chip containing 13217 distinct Entrez gene IDs (formerly known as LocusLink) and 15888 distinct unigene IDs, the remainders are incompletely annotated IMAGE clones. Probe preparation and hybridization were performed as follows. The total RNA (15-50 ãÃg in 15.5 ãÃl) was incubated with amine-modified random primer (2 ãÃg/ãÃl, 2 ãÃl) and RNase inhibitor (5 units/ãÃl, 1 ãÃl) at 70 äaC for 10 min. Primer-RNA solution was then incubated at 42 äaC for 2 hr with the reverse transcriptase mix containing 5X first-strand buffer, 50X aa-dUTP/dNTPs (25 mM dATP, 25 mM dGTP, 25 mM dCTP, 15 mM dTTP and 10 mM aminoallyl dUTP), 0.1 M DDT, and Superscript II reverse transcriptase. The cDNA were labeled with NHS-ester Cy3 or Cy5 dye in the presence of 1 M sodium bicarbonate. Array slides placed in a hybridization chamber (Corning, Corning, NY) were incubated at 42 äaC for 16-24 hr, and successively washed with 0.5X SSC, 0.01% SDS, and 0.06X SSC at room temperature for 10 min each. Arrays were scanned with a GenePix 4000A scanner (Axon, Foster City, CA), and the resulting images were analyzed using IPlab (Fairfax, VA) and a FileMaker Pro 5 (Santa Clara, CA) relational database designed by Zedong Chen, NHGRI. Following background subtraction and normalization, a calculated ratio of Cy3 to Cy5 signal intensities was used to define the relative increase or decrease of a particular transcript. Ratios were calculated only from those spots with a combined ratio quality above 0.3.
2010-07-01 | E-GEOD-5902 | biostudies-arrayexpress
Project description:Identification of hemoglobin-derived fragments generated in the anterior midgut of Rhodnius prolixus in vivo at 14 days post-feeding. The results allowed to draw the hemoglobin cleavage map by midgut-associated peptidases.
2024-04-28 | PXD044590 | Pride
Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly though a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis. Incorportation of ChIP-seq data of Sox9 and histone modification marks for chromatin status together with microrarray gene expression profiling in neonatal mice chondrocytes to uncover Sox9 regulatory system
2015-07-01 | E-GEOD-69108 | biostudies-arrayexpress
Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly though a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis. Incorportation of ChIP-seq data of Sox9 and histone modification marks for chromatin status together with micorarray gene expression profiling in neonatal mice chondrocytes to uncover Sox9 regulatory system. Overexpression of Sox9 with a control of EGFP in human fibroblasts to identify the direct targets of Sox9 regulatory system
2015-07-01 | E-GEOD-69109 | biostudies-arrayexpress
Project description:To evaluate the roles of DUOX2 in flagellin- induced inflammatory response in mouse nasal mucosa. Wild type (Duox2+/+) and Duox2 knockout (Duox2-/-) mice were stimulated with 1 M-NM-<g/ml of flagellin for 4h. 422 genes (> 2 fold) were up-regulated in nasal mucosa of Duox2+/+ that was treated with flagellin and the full list of genes is presented in Supplemental Table II. These genes included the following defense- and immune response-related genes : Cytokine/chemokine-related genes (CCL20, CCR2, CCR5, CXCL2, CXCL5, CXCL9, CXCL16, IL18RAP, TNFAIP2, IL1B EAR2, FPR1), Granulocyte-related genes (IL8RB, MPO, PRG2, PPBP, PRG3), interferon-related genes (IFITM6, IFI47), macrophage related genes (IL1B, S100A9), and T-cell mediated immune response related genes (H2-Q6, IL1F9). In addition, signal transduction (PPBP, OLFR60, P2RY10) and cell adhesion (SELL, SELP, ICAM1, DSG1A, DSG3, VCAM1) related genes were also increased by flagellin treatment. These genes were selected based on the biological processes and molecular functions of their gene ontology. However, the increase of inflammation and immune response related genes by flagellin treatment were diminished in the nasal mucosa of the Duox2-/- mice compared with that of Duox2+/+ mice. Wild type (Duox2+/+) and Duox2 knockout (Duox2-/-) mice received either PBS (control) or flagellin (5 ug/ml) intranasally for 4h.
2013-12-18 | E-GEOD-26135 | biostudies-arrayexpress
Project description:Nasal septum deviation (NSD) is a common abnormality of the septal cartilage often associated with disordered breathing. The etiology of NSD is unknown. BMP7 neural crest-knockout mice, a well-characterized model for midfacial hypoplasia and nasal airway obstruction, develops a deviated septum by 4 weeks of age. Using comparative gene expression, quantitative proteomics, and immunofluorescence analysis we investigated the septum prior, immediately preceding, and with established deviation. We provide a detailed description of cellular and molecular changes leading to septum deviation, including changes to extracellular matrix organization, cell metabolism, and chondrocyte differentiation. Loss of BMP7 was associated with acquisition of elastic cartilage properties, a switch to glucose metabolism, and molecular characteristics commonly associated with osteoarthritis (OA). Many alterations preceded the deviation establishing that molecular changes to chondrocyte properties predispose to the deviation. Interestingly, NSD was associated with a persistent increase in BMP2. Genetic reduction of BMP2 in BMP7ncko mice restores WNT signalling, energy metabolism, and rescues NSD, showing the importance of balanced BMP signaling for normal cartilage. Many of the cellular and molecular changes have been described for knee osteoarthritis, suggesting that these two pathologies might have a similar underlying etiology.
2021-04-30 | PXD024813 | Pride
Project description:Splenic CD11b+ and CD4+ cells were isolated from Dnmt3a+/+ or Dnmt3aR878/+ mice using LS columns on the magnetic field of QuadroMACS Separator according to the manufacturer’s instructions (Miltenyi Biotec), and the High-Molecular-Weight (HMW) DNA of cells were isolated using MagAttract HMW DNA Kit according to the manufacturer’s instructions (Qiagen). WGBS was performed using the Zymo-Seq WGBS Library Kit (Zymo research) according to the manufacturer’s recommendations at the High Throughput Sequencing Core of Children’s Hospital of Philadelphia, PA, USA. The sequence was generated on Illumina NovaSeq 6000 using NovaSeq 6000 S4 Reagent Kit v1.5 (200 cycles) at 40X coverage
2024-06-04 | GSE255947 | GEO
Project description:Retinal ganglion cell (RGC) death is the final consequence of many blinding diseases, where there is considerable variation in the time course and severity of RGC loss. Indeed, this process appears to be influenced by a wide variety of genetic and environmental factors. In this study we explored the genetic basis for differences in ganglion cell death in two inbred strains of mice. We found that RGCs are more susceptible to death following optic nerve crush in C57BL/6J mice (54% survival) than in DBA2/J mice (62% survival). Using the Illumina Mouse-6 microarray, we identified 1,580 genes with significant change in expression following optic nerve crush in these two strains of mice. Our analysis of the changes occurring after optic nerve crush demonstrated that the greatest amount of change (44% of the variance) was due to the injury itself. This included changes associated with ganglion cell death, reactive gliosis, and abortive regeneration. The second pattern of gene changes (23% of the variance) was primarily related to differences in gene expressions observed between the C57BL/6J and DBA/2J mouse strains. The remaining changes in gene expression represent interactions between the effects of optic nerve crush and the genetic background of the mouse. We extracted one genetic network from this dataset that appears to be related to tissue remodeling. One of the most intriguing sets of changes included members of the crystallin family of genes, which may represent a signature of pathways modulating the susceptibility of cells to death. Differential responses to optic nerve crush between two widely used strains of mice were used to define molecular networks associated with ganglion cell death and reactive gliosis. These results form the basis for our continuing interest in the modifiers of retinal injury. 18 Samples: 9 per strain (C57BL/6J & DBA/2J); 3 conditions per strain
2010-08-19 | E-GEOD-17117 | biostudies-arrayexpress
Project description:We applied the NanoString gene expression platform to total RNA isolated from the vomeronasal mucosa of mice of a strain (M-bM-^HM-^FH2Mv) in which we had excised with chromosome engineering a 530 kb genomic region that encompasses nine non-classical class I MHC genes that are expressed specifically in vomeronasal sensory neurons. At three weeks of age, there is no difference of expression for all Vmn2r genes tested; and at eight weeks of age, there is no difference of expression for the majority of Vmn2r genes. We designed NanoString probes for one third of the mouse Vmn2r gene repertoire, based on the reference C57BL/6 genome sequence. CodeSet Chanel includes probes for 46 Vmn2r genes and nine non-classical class I MHC H2-Mv genes that are expressed specifically in mouse vomeronasal sensory neurons. Results were analyzed with tTREAT.
2014-04-09 | E-GEOD-54061 | biostudies-arrayexpress