Project description:Vascular smooth muscle cells (VSMC) and endothelial cells (EC) were stimulated with factor VII activating protease and transcriptional changes were determined.

2017-10-13 | E-MTAB-5592 | biostudies-arrayexpress

Role of EVs in inflammation propagation and oxidative stress during vascular calcification

Project description:Role of EVs in inflammation propagation and oxidative stress during vascular calcification

2022-05-19 | PXD029441 | Pride

Beiging of perivascular adipose tissue regulates its inflammation and vascular remodeling

Project description:Although inflammation plays critical roles in the development of atherosclerosis, its regulatory mechanisms remain incompletely understood. Perivascular adipose tissue (PVAT) has been reported to undergo inflammatory changes in response to vascular injury. Here, we showed that vascular injury induced the beiging (brown adipose tissue-like phenotype change) of PVAT, which fine-tunes inflammatory response and thus vascular remodeling as a protective mechanism. In a mouse model of endovascular injury, macrophages accumulated in PVAT, causing beiging phenotype change. Inhibition of PVAT beiging by genetically silencing PRDM16, a key regulator to beiging, exacerbated inflammation and vascular remodeling following injury. Conversely, activation of PVAT beiging attenuated inflammation and pathological vascular remodeling. Single-cell RNA sequencing revealed that beige adipocytes abundantly expressed neuregulin 4 (Nrg4) which critically regulated alternative macrophage activation. Importantly, significant beiging was observed in the diseased aortic PVAT in patients with acute aortic dissection. Taken together, vascular injury induced the beiging of adjacent PVAT with macrophage accumulation, where NRG4 secreted from the beige PVAT facilitated alternative activation of macrophages, leading to the resolution of vascular inflammation. Our study demonstrated the pivotal roles of PVAT in vascular inflammation and remodeling and will open a new avenue for treating atherosclerosis.

2022-06-21 | GSE206399 | GEO

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

Project description:Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

| PRJNA555585 | ENA

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.

2024-06-29 | GSE236167 | GEO

Limited systemic sclerosis patients with PAH show biomarkers of inflammation and vascular injury

Project description:Limited systemic sclerosis patients with pulmonary arterial hypertension show biomarkers of inflammation and vascular injury Forty-nine PBMC samples were obtained from 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls; three subjects provided PBMCs one year later. Genome-wide gene expression was measured for each sample. Gene expression clearly distinguished lSSc samples from healthy controls, and separated lSSc-PAH from lSSc-NoPAH patients. The gene expression and cytokine profiles of lSSc-PAH patients suggest the presence of activated monocytes, and show markers of vascular injury and inflammation. Sample vs reference, total RNA isolated from peripheral blood mononuclear cells (PBMC), 21 lSSc subjects without PAH (lSSc-noPAH), 15 lSSc subjects with PAH (lSSc-PAH), and 10 healthy controls

2010-10-27 | E-GEOD-19617 | biostudies-arrayexpress

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