Unknown,Transcriptomics,Genomics,Proteomics

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Colony stimulating factor 2 causes changes in the transcriptome of the bovine preimplantation embryo

ABSTRACT: The objective of this study was to identify changes on the CSF2 embryo transcriptome that make them more able to become a blastocyst and more likely to survive after transfer. Embryos were treated with CSF2 at day 5 after fertilization and at day 6 morulae and blastocysts were select for the microarray analysis. A total of 160 genes that had a 1.5-fold difference in expression and a significance of P M-bM-^IM-$ 0.05 could be annotated. Analysis of the data identified 13 biological process ontologies that could be grouped into four functional groups (development and differentiation process, cell communication, apoptosis and cell adhesion). Experimental conditions: CSF2 treated vs. CSF2 nontreated bovine in vitro produced preimplantation embryos. Biological replicates: CSF2 treated vs. nontreated bovine preimplantation embryos were used in a dye switch two-color microarray experimental design. Ratio data was not used in these experiments.

ORGANISM(S): Bos taurus

SUBMITTER: Peter Hansen

PROVIDER: E-GEOD-22579 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The gene expression of murine splenic myeloid derived suppressor cells treated with Tff2 is characterized. The motivation of the study originates in the fact that Gr1+Cd11b+ myeloid-derived suppressor cells (MDSCs), which resemble immature myeloid cells (IMCs), expand during cancer in response to inflammatory cytokines and accumulate in the spleen. MDSCs promote neoplastic progression through their suppression of anti-tumourigenic cytotoxic T-cells. MDSCs are also rapidly expanded following acute insults, but in cancer as opposed to acute inflammation, MDSCs persist. It is now recognized that a vagally-mediated, anti-inflammatory reflex arc promoting acetylcholine secretion by Cd4+ (Cd44hiSelllo) T cells, is necessary for a return to homeostasis after an acute insult. Failure of this restorative neural circuit might contribute to unabated procarcinogenic inflammation, with the chronic expansion of MDSCs driving carcinogenesis. Trefoil factor 2 (Tff2) is a secreted anti-inflammatory peptide produced by both epithelial cells and a small subset of splenic T cell. In this study, we show that splenic Tff2 is induced in vagally-modulated memory T cells to suppress the expansion of MDSCs in response to chemical and carcinogenic injury. Deletion of Tff2 interrupts this anti-inflammatory neural arc and leads to expanded MDSCs and a dramatically increased incidence of colorectal cancer. Tff2 directly suppresses proliferation of myeloid progenitors, in a large part through upregulation of cell-bound Apolipoprotein E (ApoE), which has previously been shown to suppress proliferation of haematopoietic stem and progenitor cells. The predisposition to inflammation-associated cancer can be rescued through transgenic overexpression of splenic Tff2, adenoviral transfer of Tff2 expression or transplantation of Tff2-expressing haematopoietic cells. Thus, Tff2 production in memory T cells, is regulated by the vagus nerve, plays a central role in arresting procarcinogenic MDSC proliferation, and offers a novel approach to the prevention and treatment. A. Gr1+Cd11b+ splenic cells from Tff2-/- mice treated with Csf2 (n=4). B. Gr1+Cd11b+ splenic cells from Tff2-/- mice treated with Tff2 and Csf2 (n=4).

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Colony stimulating factor 2 causes changes in the transcriptome of the bovine preimplantation embryo

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