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Association of microRNAs with CD68 and NOS2 in IBD tissues.

ABSTRACT: We analyzed the association of CD68 and NOS2 mRNA expression with microRNAs in IBD tissues. For this analysis, data was LOESS normalized in R. Data was then imported into Partek Genomics Suite and Batch effects caused by day to day variability (Dategroup of array charateristic) were corrected. We did not have mRNA expression data for CD68 and NOS2 for all of the samples, therefore those samples were not used for analysis. We identified several microRNAs associated with CD68 and NOS2 expression.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE29703 | GEO | 2012/08/01

SECONDARY ACCESSION(S): PRJNA141191

REPOSITORIES: GEO

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Association of microRNAs with CD68 and NOS2 in IBD tissues.

Project description:We analyzed the association of CD68 and NOS2 mRNA expression with microRNAs in IBD tissues. For this analysis, data was LOESS normalized in R. Data was then imported into Partek Genomics Suite and Batch effects caused by day to day variability (Dategroup of array charateristic) were corrected. We did not have mRNA expression data for CD68 and NOS2 for all of the samples, therefore those samples were not used for analysis. We identified several microRNAs associated with CD68 and NOS2 expression. Total mRNA was extracted from colon tissue that was flash frozen immediately after surgery. A total of 114 tissues were used for microarray analysis. Briefly, 5 ug of RNA were biotin labeled and hybridized to OSU-CCC microRNA microarrays version 2.0. We then analyzed associations with CD68 and NOS2 mRNA expression.

2012-07-31 | E-GEOD-29703 | biostudies-arrayexpress

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Ptch1+/- Nos2-/- medulloblastomas

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Project description:The Ptch1+/- strain constitues an established mouse model for the Shh-driven type of medulloblastoma. Combined Ptch1+/- Nos2-/- mice show a two-fold increased incidence for this tumor. Here, the impact of Nos2 inactivation on medulloblastoma development was investigated by gene expression profiling of tumor samples as well as healthy cerebellum at different ages and genotypes. Medulloblastoma samples from three Ptch1+/- and six combined Ptch1+/- Nos2-/- mice were analyzed. Healthy cerebellum taken from mice at postnatal day nine, six weeks after birth, and about 1 year of age were analyzed for wildtype animals and the genotypes Ptch1+/-, Ptch1+/- Nos2-/-, and Nos2-/-. The cerebellar developmental stages at six weeks and one year were measured in three biological replicates, while samples taken at postnatal day six consisted of pooled individual specimen. These were measured in three replicates being amplified and labelled in separate reactions. All samples were subjected to two-color hybridizations against Universal Reference RNA (Stratagene) with color-switch experiments yielding two technical replicates, respectively.

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Expression data from targeting of NOS2 in glioma stem cells

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Expression data from from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin or saline challenge

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Project description:Tristetraprolin (TTP), encoded by the Zfp36 gene, is a zinc-finger protein that regulates RNA stability primarily through association with 3’ untranslated regions (3’UTRs) of target mRNAs. While TTP is expressed abundantly in the intestines, its function in intestinal epithelial cells (IECs) is unknown. Here we used a cre-lox system to remove Zfp36 in the mouse epithelium to uncover a role for TTP in IECs and to identify target genes in these cells. While TTP was largely dispensable for establishment and maintenance of the colonic epithelium, we found an expansion of the proliferative zone and an increase in goblet cell numbers in the colon crypts of Zfp36ΔIEC mice. Furthermore, through RNA-sequencing of transcripts isolated from the colons of Zfp36fl/fl and Zfp36ΔIEC mice, we found that expression of inducible nitric oxide synthase (iNos or Nos2) was elevated in TTP-knockout IECs. We demonstrate that TTP interacts with AU-rich elements in the Nos2 3’UTR and suppresses Nos2 expression. In comparison to control Zfp36fl/fl mice, Zfp36ΔIEC mice were less susceptible to dextran sodium sulfate (DSS)-induced acute colitis. Together, these results demonstrate that TTP targets Nos2 expression in IECs and aggravates acute colitis.

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