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

Cryo-EM structures of the human SIN3B histone deacetylase complex unveils assembly, enzymatic activation and histone lysine selection mechanisms

Project description:Lysine acetylation is a key transcriptional activating signalling modification occurring at the flexible ends of the histone proteins within the nucleosome, which is the basic unit of chromatin. Several histone deacetylase complexes in human fine tune these modifications thereby regulating the transcriptional output of each gene. Although histone deacetylase complexes are crucial in defining transcriptional programs during cell differentiation and cell cycle the structural information and mechanisms of actions of these holoenzymes is poor. Here we present the structure of the SIN3B histone deacetylase complex in apo form and in complex with an acetyl-lysine mimic compound, showing insights into its subunit architecture, catalytic regulation, substrate recognition and targeting to cell cycle genes.

2023-03-31 | PXD040006 | Pride

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

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

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

Project description:Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

| PRJNA555585 | ENA

Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (microarray)

Project description:Macrophages, a key cellular component of inflammation, become functionally polarized in a signal- and context-specific manner. Th2 cytokines such as IL-4 polarize macrophages to a state of alternative activation that limits inflammation and promotes wound healing. Alternative activation is mediated by a transcriptional program that is influenced by epigenomic modifications including histone acetylation. To determine if Histone Deacetylase 3 (HDAC3) has a role in macrophage polarization including alternative activation, we have performed global gene expression analysis in macrophages with and without HDAC3 and with or without IL-4 exposure. From this data, we conclude that macrophages lacking histone deacetylase 3 (HDAC3) display a polarization phenotype similar to IL-4 induced alternative activation and furthermore are hyper-responsive to IL-4 stimulation. Mouse bone marrow derived macrophages were obtained from both control and HDAC3 KO animals and treated with vehicle control (BSA) or IL-4 for 24 hours. RNA was isolated and subjected to analysis using an Agilent Whole Genome Microarray Kit.

2011-11-10 | E-GEOD-33608 | biostudies-arrayexpress

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