Ontology highlight
ABSTRACT:
PROVIDER: PRJNA967488 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24451120_1.fastq.gz | Fastqsanger.gz | |||
| SRR24451120_2.fastq.gz | Fastqsanger.gz | |||
| SRR24451121_1.fastq.gz | Fastqsanger.gz | |||
| SRR24451121_2.fastq.gz | Fastqsanger.gz | |||
| SRR24451122_1.fastq.gz | Fastqsanger.gz |
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Project description:Cirrhosis profoundly impacts extrahepatic vasculature, particularly altering the portal venous system (PVS), leading to increased portal pressure, portosystemic collaterals, and portal vein thrombosis, which heightens morbidity and reduced survival in patients with liver disease. Despite extensive research on intrahepatic vasculature in cirrhosis, understanding of extrahepatic changes in the splanchnic territory at the molecular level remains limited. The distinct characteristics of the PVS suggest a unique endothelial profile crucial for elucidating vascular dysfunction in liver diseases. However, current research is hampered by the inaccessibility of the portal vein and imperfect preclinical models. Here, we aim to isolate and immortalize primary human portal vein endothelial cells (hPVECs) to enhance understanding of pathophysiological changes during liver disease and establish a platform for future drug testing.
2025-12-02 | GSE296600 | GEO
Project description:Portal vein thrombosis (PVT) is a prevalent thrombotic complication in cirrhosis, yet its pathophysiology remains elusive, hindering effective treatment strategies. Unlike thrombosis in other vascular beds, anticoagulation often fails to achieve complete recanalization in PVT, highlighting the need of alternative therapeutic approaches. We investigated portal vein endothelium involvement in PVT pathogenesis, identifying potential therapeutic targets. We isolated for the first time primary human portal vein endothelial cells (PVEC) from explanted livers of cirrhotic patients with and without PVT, as well as from a control group without portal hypertension and conducted RNA sequencing. Transcriptomic analysis unveiled endothelial-to-mesenchymal transition (EndMT) pathway as a key mechanism underlying PVT in cirrhosis, predominantly induced through TGFβ/SMAD mechanism. Remarkably, coagulation markers remained unaffected. In silico drug repurposing identified statins as potential agents targeting these alterations. Our study elucidates significant endothelial changes in the portal vein of cirrhotic patients, particularly pronounced in those with PVT, with EndMT emerging as a pivotal process. Simvastatin emerges as a promising therapeutic option for PVT treatment and prevention by modulating EndMT in PVEC.
2025-12-02 | GSE261883 | GEO
Project description:Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear. We used microarrays to identify the functions of genes expressed in blood samples from patients with IPH.
2015-06-06 | GSE69601 | GEO
Project description:Gut-derived microbial metabolites have been shown to play key roles in human physiology and disease. However, establishing mechanistic links between gut microbial metabolites and disease pathogenesis in animal models presents many challenges. The major route of absorption for microbe-derived small molecules is venous drainage via the portal vein to the liver. In the event of extensive liver first pass- or presystemic hepatic metabolism, the route of administration of these metabolites becomes critical. Here we describe a novel portal vein cannulation technique using a subcutaneously implanted osmotic pump to achieve continuous portal vein infusion in mice. First, the microbial metabolite trimethylamine (TMA) was administered over 4 weeks and compared to a vehicle control. Using a liquid chromatography-tandem mass spectrometry (LC-MS/MS), an increase in peripheral plasma levels of TMA and its host liver-derived co-metabolite trimethylamine-N-oxide (TMAO) were observed in a sexually-dimorphic manner. Next, 4-hydroxyphenylacetic acid (4-HPAA), a structurally-distinct microbial metabolite that undergoes extensive hepatic first pass metabolism, was administered portally to examine its effects on hepatic gene expression. Peripheral plasma levels showed no difference in free or total 4-HPAA. However, while liver tissue demonstrated no difference in free 4-HPAA, total levels were increased when compared to the control group. More importantly, significant changes were observed in hepatic gene expression using an unbiased RNA sequencing approach. Collectively, this work describes a novel method for administering gut microbe-derived metabolites via the portal vein, mimicking their physiologic delivery in vivo.
2021-05-10 | GSE159775 | GEO
Project description:Germ-free mice are an indispensable tool in studying the gut microbiome and its effects on host physiology, though they are phenotypically different than their conventional counterparts. While antibiotic mediated microbiota depletion in conventional mice mimics the germ-free state, the scope of these reversible changes is unknown. We demonstrate robust hepatic transcriptomic alterations after antibiotic-mediated microbiota depletion together with depletion of luminal and portal vein levels of SCFAs though hepatic histone acetylation states remained largely unchanged.
2023-01-25 | GSE144266 | GEO
Project description:Idiopathic portal hypertension (IPH) is characterized by portal hypertension due to obstruction or stenosis of the intrahepatic peripheral portal branches. Researchers have suggested that IPH may be attributed to intrahepatic peripheral portal vein thrombosis, splenic factors, abnormal autoimmunity, and related factors, however, the etiology of IPH remains unclear. We used microarrays to identify the functions of genes expressed in blood samples from patients with IPH. In order to examine the specific expression of genes in patients with IPH, we analyzed blood samples from three patients with IPH and three healthy volunteers as control using DNA microarrays.
2015-06-06 | E-GEOD-69601 | biostudies-arrayexpress
Project description:<p><b>Overview:</b><br/> <u>Our overall long-term goal is to determine risk factors for the complex (multifactorial) disease, venous thromboembolism (<b>VTE</b>), that will allow physicians to stratify individual patient risk and target VTE prophylaxis to those who would benefit most.</u> In this genome-wide association case-control study (1300 cases and 1300 controls) we hope to identify susceptibility variants for VTE.</p> <p>Mutations within genes encoding for important components of the anticoagulant, procoagulant, fibrinolytic, and innate immunity pathways are risk factors for VTE. We hypothesize that other genes within these four pathways or within other pathways also are VTE disease-susceptibility genes. Therefore, we performed a genome wide association (GWA) screen and analysis using the Illumina 660W platform to identify SNPs within 1,300 clinic-based, non-cancer VTE cases primarily from Minnesota and the upper Midwest USA, and 1300 clinic-based, unrelated controls frequency-matched on patient age, gender, myocardial infarction/stroke status and state of residence.</p> <p>This is a subset of a slightly larger candidate gene study using 1500 case-control pairs to identify haplotype-tagging SNPs (<b>ht</b>-SNPs) in a large set of candidate genes (n~750) within the anticoagulant, procoagulant, fibrinolytic, and innate immunity pathways.</p> <p><b>Study Populations.</b><br/> <b><u>Cases</u>.</b> VTE cases were consecutive Mayo Clinic outpatients with objectively-diagnosed deep vein thrombosis (DVT) and/or pulmonary embolism (PE) residing in the upper Midwest and referred by Mayo Clinic physician to the Mayo Clinic Special Coagulation Laboratory for clinical diagnostic testing to evaluate for an acquired or inherited thrombophilia, or to the Mayo Clinic Thrombophilia Center. Any person contacted to be a control but discovered to have had a VTE was evaluated for inclusion as a case. Cases were primarily residents from Minnesota, Wisconsin, Iowa, Michigan, Illinois, North or South Dakota, Nebraska, Kansas, Missouri and Indiana. A DVT or PE was categorized as objectively diagnosed when (a) confirmed by venography or pulmonary angiography, or pathology examination of thrombus removed at surgery, or (b) if at least one non-invasive test (compression duplex ultrasonography, lung scan, computed tomography scan, magnetic resonance imaging) was positive. A VTE was defined as: <ol> <li>Proximal leg deep vein thrombosis (DVT), which includes the common iliac, internal iliac, external iliac, common femoral, superficial [now termed "femoral"] femoral, deep femoral [sometimes referred to as "profunda" femoral] and/or popliteal veins. (Note: greater and lesser saphenous veins, or other superficial or perforator veins, were not included as proximal or distal leg DVT).</li> <li>Distal leg DVT (or "isolated calf DVT"), which includes the anterior tibial, posterior tibial and/or peroneal veins. (Note: gastrocnemius, soleal and/or sural [e.g., "deep muscular veins" of the calf] vein thrombosis was not included as distal leg DVT).</li> <li>Arm DVT, which includes the axillary, subclavian and/or innominate (brachiocephalic) veins. (Note: jugular [internal or external], cephalic and brachial vein thrombosis was not included in "arm DVT").</li> <li>Hepatic, portal, splenic, superior or inferior mesenteric, and/or renal vein thrombosis. (Note: ovarian, testicular, peri-prostatic and/or pelvic vein thrombosis was not included).</li> <li>Cerebral vein thrombosis (includes cerebral or dural sinus or vein, saggital sinus or vein, and/or transverse sinus or vein thrombosis).</li> <li>Inferior vena cava (IVC) thrombosis</li> <li>Superior vena cava (SVC) thrombosis</li> <li>Pulmonary embolism</li> </ol> </p> <p>Patients with VTE related to active cancer, antiphospholipid syndrome, inflammatory bowel disease, vasculitis, a rheumatoid or other autoimmune disorder, a vascular anomaly (e.g., Klippel-Trénaunay syndrome, etc.), heparin-induced thrombocytopenia, or a mechanical cause for DVT (e.g., arm DVT or SVC thrombosis related to a central venous catheter or transvenous pacemaker, portal and/or splenic vein thrombosis related to liver cirrhosis, IVC thrombosis related to retroperitoneal fibrosis, etc.), with hemodialysis arteriovenous fistula thrombosis, or with prior liver or bone marrow transplantation were excluded. </p> <p><b><u>Controls</u>.</b> A Mayo Clinic outpatient control group was prospectively recruited for this study. Controls were frequency-matched on the age group (18-29, 30-39, 40-49, 50-59, 60-69, 70-79, and 80+ years), sex, myocardial infarction/stroke status, and state of residence distribution of the cases. We selected clinic-based controls using a controls' database of persons undergoing general medical examinations in the Mayo Clinic Departments of General Internal Medicine or Primary Care Internal Medicine. Additionally persons undergoing evaluation at the Mayo Clinic Sports Medicine Center, and the Department of Family Medicine were screened for inclusion as controls.</p> <p>This study is part of the Gene Environment Association Studies initiative (GENEVA, <a href="http://www.genevastudy.org" target="_blank">http://www.genevastudy.org</a>) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to venous thrombosis through large-scale genome-wide association studies of 1,300 clinic-based, VTE cases and 1300 clinic-based, unrelated controls. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.</p>
| phs000289 | dbGaP
Project description:Whereas the cellular basis of the hematopoietic stem cell (HSC) niche in the bone marrow has been characterized, the nature of the fetal liver (FL) niche is not yet elucidated. We show that Nestin+NG2+ pericytes associate with portal vessels, forming a niche promoting HSC expansion. Nestin+NG2+ cells and HSCs scale during development with the fractal branching patterns of portal vessels, tributaries of the umbilical vein. After closure of the umbilical inlet at birth, portal vessels undergo a transition from Neuropilin-1+Ephrin-B2+ artery to EphB4+ vein phenotype, associated with a loss of peri-portal Nestin+NG2+ cells and emigration of HSCs away from portal vessels. These data support a model in which HSCs are titrated against a peri-portal vascular niche with a fractal-like organization enabled by placental circulation. Characterization of the transcriptome of fetal liver and adult bone marrow niche using RNA-seq
2015-12-03 | E-GEOD-72341 | biostudies-arrayexpress
Project description:CNV analysis of hepatocellular carcinoma with portal vein tumor thrombosis
| PRJNA309947 | ENA