Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA381207 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome-wide SNP analysis of the Systemic Capillary Leak Syndrome (Clarkson disease)
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Project description:Studies in the pathogenesis of systemic capillary leak syndrome (SCLS, Clarkson disease)
| PRJNA955365 | ENA
Project description:Studies in the pathogenesis of systemic capillary leak syndrome (SCLS, Clarkson disease)
| PRJNA955366 | ENA
Project description:The Systemic Capillary Leak Syndrome (SCLS) is an extremely rare and potentially life-treating vascular disorder of unknown etiology. SCLS is characterized by dramatic and transient episodes of hypotensive shock and edema due to plasma leakage into peripheral tissues. The disorder has garnered increased attention during the last several years because of the resemblance of its initial presentation to more common disorders such as systemic anaphylaxis, sepsis, and acute infections with the Ebola/Marburg family of filoviruses. Although approximately 70-80% of patients with SCLS have a concurrent monoclonal gammopathy of unknown significance (MGUS), any contribution of the paraprotein to acute flares is unknown. To identify circulating factors that contribute to the onset of acute SCLS crises, we performed transcriptomic profiling of paired peripheral blood mononuclear cell fractions obtained from patients during acute attacks and convalescent intervals using microarray. 61 genes were significantly up- or downregulated more than 2.5 fold in acute samples relative to baseline. One of the most upregulated genes was ADM, which encodes the vasoactive peptide adrenomedullin. The ADM surrogate pro-ADM was markedly elevated in SCLS acute sera compared to remission samples or sera from healthy controls. Monocytes and endothelial cells (ECs) from SCLS subjects expressed significantly more ADM in response to proinflammatory stimuli compared to healthy control cells. Application of ADM to ECs exerted protective effects on vascular barrier function. These results suggest a pathogenic contribution of ADM to the profound pressor-resistant hypotension that characterizes the initial stages of SCLS.
2018-03-31 | GSE97287 | GEO
Project description:Capillary leak is a hallmark of acute and chronic inflammatory conditions and represents a critical driver of organ dysfunction and poor clinical outcomes. Despite its clinical relevance, the mechanisms governing endothelial destabilization under inflammatory conditions remain incompletely understood. In this study, we investigated the endothelial response to inflammation using a dynamic human in vitro model, in which human umbilical vein endothelial cells (HUVECs) were cultured in the presence of lipopolysaccharide (LPS)–stimulated human peripheral blood mononuclear cells (PBMCs) to mimic systemic inflammation. Under these conditions, endothelial cells exhibited a pronounced inflammatory response characterized by loss of barrier integrity and the formation of capillary leak–like structures. Separated transcriptomic pathway analyses of HUVECs and PBMCs identified a strong activation of cytokine-driven signalling networks, with the IL-17 pathway emerging as a dominant regulator of endothelial dysfunction, alongside TNF and JAK–STAT signalling. Targeted pharmacological inhibition demonstrated that blockage of IL-17 signalling most effectively stabilized the endothelial layer and mitigated leak-like morphology compared to inhibition of other pathways. However, endothelial barrier function was only partially restored, indicating persistent dysfunction despite IL-17 pathway suppression. Together, these findings position IL-17 as a key driver of inflammation-induced capillary leak while highlighting the multifactorial nature of endothelial destabilization. This work underscores the necessity of addressing complex immune–endothelial interactions to develop effective strategies for preventing inflammation-induced vascular leakage.
2026-04-06 | GSE326579 | GEO
Project description:Pseudoexfoliation syndrome (PEX) is a systemic disorder that manifests as a fluffy, proteinaceous fibrillar material throughout the body. In the eye, such deposits result in glaucoma (PEXG), due to impeding aqueous humor outflow. When a patient presents acute glaucoma, it is necessary to remove some of the aqueous fluid within the eye to relief pain and pressure. This label free proteomics dataset was collected from human donors during cataract surgery. The aqueous humor was collected during essential ophthalmic procedures that allowed paracentesis after obtaining informed consents from human subjects without collecting identifiers, but all disease and medication history were collected. The sample collection included non-glaucomatous controls (CTL-GC), those with pseudoexfoliation syndrome (PEX-GC), and synthesized GC-Globulin pure protein (GC-Pure). Approximately 50-120 ul volume of AH was collected by paracentesis and stored in -80C immediately upon acquisition until analysis. Protein extraction was carried out by homogenization of the tissue in extraction buffer (TEAB, NaCl and SDS). Protein amounts were estimated and normalized to 10 ug across experimental samples. Samples were reduced using TCEP, alkylated with iodoacetamide and digested overnight with trypsin. Untargeted liquid chromatography-mass spectrometry was performed on an Easy nLC 1000 liquid chromatograph coupled to a QExactive mass spectrometer (LC-MS/MS). Data analysis was performed using Proteome Discoverer 3.0 and Graph Pad Prism 10. Each sample was run three separate times.
Raw mass spectrometry data files were analyzed using Proteome Discoverer 3.0. The human proteome was downloaded from UniProt and used as the target database for protein identification. Max missed cleavage site was set to 2 and minimum peptide length to 6. Precursor Mass Tolerance was set to 10ppm and Fragment Mass Tolerance to 0.02 Da. Post-translational modifications for experimental proteins included oxidation, acetylation, and carbamidomethylation. The normalization was set to total peptide amount and confidence to low.
2023-12-18 | MSV000093682 | MassIVE
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:Renal systems biology of patients with systemic inflammatory response syndrome
| PRJNA280230 | ENA
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description: Not available
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