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PARP15 promotes vascular barrier integrity in inflammation

ABSTRACT: PARP15 promotes vascular barrier integrity in inflammation

PROVIDER: PRJNA989163 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25079303_1.fastq.gz	Fastqsanger.gz
	SRR25079303_2.fastq.gz	Fastqsanger.gz
	SRR25079304_1.fastq.gz	Fastqsanger.gz
	SRR25079304_2.fastq.gz	Fastqsanger.gz
	SRR25079305_1.fastq.gz	Fastqsanger.gz

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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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