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Apelin 13 breaks the immune cell route from lung to brain [RNA-Seq]

ABSTRACT: Apelin 13 breaks the immune cell route from lung to brain [RNA-Seq]

PROVIDER: PRJNA961751 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24302372_1.fastq.gz	Fastqsanger.gz
	SRR24302372_2.fastq.gz	Fastqsanger.gz
	SRR24302373_1.fastq.gz	Fastqsanger.gz
	SRR24302373_2.fastq.gz	Fastqsanger.gz
	SRR24302374_1.fastq.gz	Fastqsanger.gz

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Apelin 13 breaks the immune cell route from lung to brain

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Apelin 13 breaks the immune cell route from lung to brain [scRNA-Seq]

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Apelin 13 breaks the immune cell route from lung to brain [RNA-Seq]

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Apelin 13 breaks the immune cell route from lung to brain [scRNA-Seq]

Project description:Apelin 13 breaks the immune cell route from lung to brain [scRNA-Seq]

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Apelin 13 breaks the immune cell route from lung to brain

Project description:This SuperSeries is composed of the SubSeries listed below.

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Apelin/APJ signaling mediated by G alpha 13 and MEF2 in endothelial cells

Project description:Evaluation of gene transcripts that are downstream of apelin/APJ signaling in HUVECs Duplicates per group, subjected to: 1) control siRNA, 2) MEF2A and MEF2C siRNA, 3) G alpha 13 siRNA, and 4) apelin and APJ siRNA

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Apelin-13 modulates the endometrial transcriptome of the domestic pig during the implantation phase of pregnancy

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Apelin absence in endothelial cells

Project description:First, transcriptome analysis of purified CD31+ endothelial cells (ECs) from VEGF-treated sprouting embryoid bodies showed angiogenesis as the top affected category when Apelin is not present. In addition, loss of Apelin resulted in the modulation of pathways in ECs related to vasculogenesis, cell adhesion and response to hypoxia. Ingenuity Pathway Analysis (IPA) further identified VEGFR pathway as the main upstream regulator affected in endothelial cells, closely followed by the TGFβ1 and TNF pathways, all reduced in the absence of Apelin. The most inhibited genes from the VEGFR pathway in the absence of Apelin are angiogenesis-related genes. Second, transcriptome analysis of CD31+/CD105+ ECs sorted from Apelin wild-type and Apln-depleted tumors found a significant decrease in processes associated with endothelial cell proliferation and angiogenesis in ECs sorted out of Apelin-depleted tumors using IPA. Further, IPA predicted a decrease in the adhesion of granulocytes and upstream regulator analysis showed that proteins of the TGF-superfamily, Inhibin-βA and TGF-β1, as well as C/EBP-alpha, β-Catenin, ErbB2 and EGFR are predicted to be inhibited upstream regulators in ECs isolated from Apelin-depleted tumors.

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2012-12-04 | E-GEOD-42343 | biostudies-arrayexpress

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