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TRAF7 is an essential regulator of vascular integrity

ABSTRACT: TRAF7 is an essential regulator of vascular integrity

PROVIDER: PRJNA955312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24164400_1.fastq.gz	Fastqsanger.gz
	SRR24164400_2.fastq.gz	Fastqsanger.gz
	SRR24164401_1.fastq.gz	Fastqsanger.gz
	SRR24164401_2.fastq.gz	Fastqsanger.gz
	SRR24164402_1.fastq.gz	Fastqsanger.gz

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Vascular integrity is essential for maintaining tissue homeostasis

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Project description:Targeted deletion of TRAF7 revealed that it is a crucial part of shear stress-responsive MEKK3-MEK5-ERK5 signaling pathway induced in endothelial cells by blood flow. Similarly, to Mekk3-, Mek5- or Erk5-deficient mice, Traf7-deficient embryos died in utero around midgestation due to impaired endothelial cell integrity. They displayed significantly lower expression of transcription factor Klf2, an essential regulator of vascular hemodynamic forces downstream of the MEKK3-MEK-ERK5 signaling pathway. Deletion of Traf7 in endothelial cells of postnatal mice was also associated with severe cerebral hemorrhage. Here, we show that besides MEKK3 and MEK5, TRAF7 associates with a planar cell polarity protein SCRIB. SCRIB binds with an N-terminal region of TRAF7, while MEKK3 associates with the C-terminal WD40 domain. Downregulation of TRAF7 as well as SCRIB inhibited fluid shear stress-induced phosphorylation of ERK5 in cultured endothelial cells. These findings suggest that TRAF7 and SCRIB may comprise an upstream part of the MEKK3-MEK5-ERK5 signaling pathway. Objective: to present first in vivo experimental evidence of TRAF7 function by using global and endothelium-specific TRAF7 knockout mice and comparing transcriptomes of developing embryos.

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Vascular integrity is essential for maintaining tissue homeostasis I

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PARP15 promotes vascular barrier integrity in inflammation

Project description:The vascular endothelial barrier, which supports balanced plasma solute and macromolecule composition, controls hemostasis, and limits leukocyte extravasation at homeostasis, is frequently disrupted in inflammation associated with sepsis and other critical illness. Monoclonal gammopathy-associated idiopathic systemic capillary leak syndrome (ISCLS, Clarkson disease) is a rare and devastating disorder characterized by relapsing-remitting episodes of spontaneous, profound microvascular hyper-permeability. A loss of function (LOF) mutation (G628R) in the mono ADP-ribosyltransferase PARP15, a protein of unknown function that is absent in mice, is associated with ISCLS and correlates with clinical markers of severe vascular leakage. In vascular endothelial cells, PARP15 suppresses cytokine-induced barrier disruption by ADP-ribosylating the scaffold protein JNK-interacting protein 3 (JIP3) and inhibiting p38 MAP kinase activation. Mice expressing human wild type (WT) PARP15 have curtailed inflammation-associated vascular leakage compared to mice expressing PARP15(G628R) in a p38-dependent fashion. Thus, PARP15 is essential for vascular endothelial barrier function under inflammatory stress.

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