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Effect of endothelial-specific endorepellin expression on gene expression of breast cancer allografts in Tie2CreER ERKi mice

ABSTRACT: Effect of endothelial-specific endorepellin expression on gene expression of breast cancer allografts in Tie2CreER ERKi mice

PROVIDER: PRJNA862283 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20637427_1.fastq.gz	Fastqsanger.gz
	SRR20637427_2.fastq.gz	Fastqsanger.gz
	SRR20637428_1.fastq.gz	Fastqsanger.gz
	SRR20637428_2.fastq.gz	Fastqsanger.gz
	SRR20637429_1.fastq.gz	Fastqsanger.gz

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Effect of endothelial-specific endorepellin expression on gene expression of breast cancer allografts in Tie2CreER;ERKi mice

Project description:To explore the translational implications of endorepellin in breast cancer, we created a double transgenic, inducible Tie2CreER;ERKi mouse line that expresses recombinant endorepellin specifically from the endothelium. We investigated the therapeutic effects of recombinant endorepellin overexpression in an orthotopic, syngeneic breast cancer allograft mouse model. Tamoxifen-induced expression of recombinant endorepellin specifically from the endothelium in Tie2CreER;ERKi mice markedly suppressed breast cancer allograft growth, hyaluronan deposition in the tumor proper and perivascular tissues, and tumor angiogenesis.

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Project description:Transcriptome analyses of organ transplants have until now usually focused on whole tissue samples containing activation profiles from different cell populations. Here, we enriched endothelial cells from rat cardiac allografts and isografts, establishing their activation profile at baseline and on day 2, 3 and 4 after transplantation. Modulated transcripts were assigned to three categories based on their regulation profile in allografts and isografts. Categories A and B contained the majority of transcripts and showed similar regulation in both graft types, appearing to represent responses to surgical trauma. By contrast, category C contained transcripts that were partly allograft-specific and to a large extent associated with interferon-ï§-responsiveness. Several transcripts were verified by immunohistochemical analysis of graft lesions, among them the matricellular protein periostin which was one of the most highly upregulated transcripts but has not been associated with transplantation previously. In conclusion, the majority of the differentially expressed genes in graft endothelial cells are affected by the transplantation procedure whereas relatively few are associated with allograft rejection. Endothelial cells were enriched from control/non-transplanted hearts and from allografts (DA to Lewis) and isografts (Lewis to Lewis) harvested at day 2, 3 and 4 after transplantation. Three biological replicates from each time point and graft type were analyzed (a total of 24 arrays). Leukocytes were enriched from allografts at day 2 (n=1), day 3 (n=2) and day 4 (n=1) after transplantation.

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MOLECULAR CHARACTERIZATION OF LIVER ALLOGRAFTS FROM OPERATIONALLY TOLERANT TRANSPLANT RECIPIENTS

Project description:This SuperSeries is composed of the following subset Series: GSE26622: MOLECULAR CHARACTERIZATION OF LIVER ALLOGRAFTS FROM OPERATIONALLY TOLERANT TRANSPLANT RECIPIENTS (Affymetrix) GSE26625: MOLECULAR CHARACTERIZATION OF LIVER ALLOGRAFTS FROM OPERATIONALLY TOLERANT TRANSPLANT RECIPIENTS (Illumina) Refer to individual Series

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Project description:Graft acceptance without the need for immunosuppressive drugs is the ultimate goal of transplantation therapy. In murine liver transplantation, allografts are accepted across major histocompatibility antigen complex barriers without the use of immunosuppressive drugs and constitute a suitable model for research on immunological rejection and tolerance. MicroRNA (miRNA) has been known to be involved in the immunological responses. In order to identify mRNAs in spontaneous liver allograft tolerance, miRNA expression in hepatic allografts was examined using this transplantation model. According to the graft pathological score and function, miR-146a, 15b, 223, 23a, 27a, 34a and 451 were upregulated compared with the expression observed in the syngeneic grafts. In contrast, miR-101a, 101b and 148a were downregulated. Our results demonstrated the alteration of miRNAs in the allografts and may indicate the role of miRNAs in the induction of tolerance after transplantation. Furthermore, our data suggest that monitoring the graft expression of novel miRNAs may allow clinicians to differentiate between rejection and tolerance. A better understanding of the tolerance inducing mechanism observed in murine hepatic allografts may provide a therapeutic strategy for attenuating allograft rejection.

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