Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA189555 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The Incidence of Thromboembolic Events in Patients with Antibodies to Heparin-PF4 after Cardiac Bypass (HIT) - RTDC 5801
| PRJNA189554 | ENA
Project description:Heparin-induced thrombocytopenia (HIT) is a common drug-induced immune disorder occurring in a subset of heparin-treated patients. Immune complexes comprising heparin, platelet factor 4 (PF4), and PF4/heparin-reactive antibodies are central to its pathogenesis. However, the role of epigenetic modification in HIT remains unexplored. Our study identified JMJD1C, a member of the lysine-specific histone demethylase 3 subfamily, as an essential regulator of PF4/heparin-specific antibody production. While JMJD1C was expressed throughout B-cell development and was dispensable for normal B-cell development, its deficiency disrupted immune tolerance and promoted production of self-reactive antibodies in systemic autoimmune diseases, including PF4/heparin-specific platelet-activating antibodies, a hallmark of pathogenic HIT antibodies. JMJD1C-deficient B cells were hyperresponsive, characterized by enhanced B-cell receptor (BCR)-induced proliferation. Transcriptomic analysis (RNA-Seq) revealed upregulation of pathways associated with BCR signaling, NF-kB activation, the cell cycle, and systemic lupus erythematosus (SLE). CUT&Tag profiling demonstrated that JMJD1C deficiency increased H3K36me1 modification at gene start sites in these pathways, indicating that epigenetic dysregulation drives B-cell hyperactivation. Importantly, transcriptional profiling and regulon analysis of B cells from HIT patients showed enrichment of BCR signaling, cell-cycle, NF-κB, and SLE-associated pathways, closely mirroring those in JMJD1C-deficient B cells. Epigenetic analyses further revealed enhanced promoter chromatin accessibility and elevated H3K36me1 deposition at promoter-TSS regions in HIT B cells. Together, these findings establish a strong molecular overlap between JMJD1C deficiency and human HIT B cells and reveal a previously unrecognized epigenetic mechanism underlying HIT pathogenesis. Our study provides the first evidence linking epigenetic regulation to HIT, offering new insights into its pathophysiology.
2026-04-14 | GSE327681 | GEO
Project description:Heparin-induced thrombocytopenia (HIT) is a common drug-induced immune disorder occurring in a subset of heparin-treated patients. Immune complexes comprising heparin, platelet factor 4 (PF4), and PF4/heparin-reactive antibodies are central to its pathogenesis. However, the role of epigenetic modification in HIT remains unexplored. Our study identified JMJD1C, a member of the lysine-specific histone demethylase 3 subfamily, as an essential regulator of PF4/heparin-specific antibody production. While JMJD1C was expressed throughout B-cell development and was dispensable for normal B-cell development, its deficiency disrupted immune tolerance and promoted production of self-reactive antibodies in systemic autoimmune diseases, including PF4/heparin-specific platelet-activating antibodies, a hallmark of pathogenic HIT antibodies. JMJD1C-deficient B cells were hyperresponsive, characterized by enhanced B-cell receptor (BCR)-induced proliferation. Transcriptomic analysis (RNA-Seq) revealed upregulation of pathways associated with BCR signaling, NF-kB activation, the cell cycle, and systemic lupus erythematosus (SLE). CUT&Tag profiling demonstrated that JMJD1C deficiency increased H3K36me1 modification at gene start sites in these pathways, indicating that epigenetic dysregulation drives B-cell hyperactivation. Importantly, transcriptional profiling and regulon analysis of B cells from HIT patients showed enrichment of BCR signaling, cell-cycle, NF-κB, and SLE-associated pathways, closely mirroring those in JMJD1C-deficient B cells. Epigenetic analyses further revealed enhanced promoter chromatin accessibility and elevated H3K36me1 deposition at promoter-TSS regions in HIT B cells. Together, these findings establish a strong molecular overlap between JMJD1C deficiency and human HIT B cells and reveal a previously unrecognized epigenetic mechanism underlying HIT pathogenesis. Our study provides the first evidence linking epigenetic regulation to HIT, offering new insights into its pathophysiology.
2026-04-14 | GSE326619 | GEO
Project description:To investigate changes in cardiac transcription profiles caused by on-pump cardiac surgery, we collected myocardial samples, prior and after grafting, from patients undergoing on-pump coronary artery bypass grafting with cardiopulmonary bypass and cardiac arrest. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Changes in transcriptional profiles can be correlated with the stress response of heart to surgery, cardiopulmonary bypass and cardiac arrest. Keywords: human, cardiac, CABG coronary surgery, gene expression, cardiopulmonary bypass. Myocardial samples were collected, prior and after grafting, from patients undergoing on-pump coronary artery bypass grafting with cardiopulmonary bypass and cardiac arrest.
2010-07-07 | E-GEOD-12486 | biostudies-arrayexpress
Project description:To investigate changes in cardiac transcription profiles caused by on-pump cardiac surgery, we collected myocardial samples, prior and after grafting, from patients undergoing on-pump coronary artery bypass grafting with cardiopulmonary bypass and cardiac arrest. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Changes in transcriptional profiles can be correlated with the stress response of heart to surgery, cardiopulmonary bypass and cardiac arrest. Keywords: human, cardiac, CABG coronary surgery, gene expression, cardiopulmonary bypass.
2010-06-22 | GSE12486 | GEO
Project description:Background: The elevated risk on and health burden of thromboembolic events necessitates development of blood-based patient risk monitoring.Objective: We explored the potential of mass spectrometry-based plasma proteomics to provide insights into underlying plasma protein signatures with treatment and occurrence of thromboembolic events.Method: Utilizing a high-throughput, data-independent acquisition, discovery-based proteomics workflow we analysed 434 plasma proteomes from different groups of individuals with elevated risk of thromboembolic events, including individuals I) on vitamin K-antagonists (VKA), II) with a prior venous thromboembolism, III) with acute cerebral venous sinus thrombosis (CVST) and IV) with SARS-CoV-2 infection. Plasma protein levels measured with MS were correlated with international prothrombin time ratio (INR) and conventional clinical laboratory measurements. Plasma profile differences between different groups were assessed using principal component analysis, moderated t-test and clustering analysis.Results: Plasma protein levels were in agreement with conventional clinical laboratory parameters, including albumin and fibrinogen. In addition, levels of vitamin K-dependent proteins inversely correlated with INR. In the individual retrospective studies, we found decreased levels of vitamin K-dependent coagulation proteins in patients on VKAs, alterations in inflammatory signatures among CVST patients and a distinctive signature indicative of SARS-CoV-2 infection. However, no protein signature associated with a thromboembolic event could be identified neither in individual nor combined retrospective studies. Conclusion: Although VKA treatment- and disease-specific signatures were captured, our study highlights that the challenges of discovering biomarkers in patients at risk of thromboembolic events lie in the heterogeneity of individual plasma profiles in relation to treatment and etiology.
2025-05-06 | PXD044173 | Pride
Project description:To determine cardiac transcription profile in acyanotic Tetralogy of Fallot patients, we collected myocardial samples immediately after institution of cardiopulmonary bypass from acyanotic Tetralogy of Fallot patients undergoing corrective surgery. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Myocardial samples were collected, immediately after institution of cardiopulmonary bypass from acyanotic Tetralogy of Fallot patients undergoing corrective surgery.
2010-02-27 | E-GEOD-14955 | biostudies-arrayexpress
Project description:To determine cardiac transcription profile in cyanotic Tetralogy of Fallot patients, we collected myocardial samples immediately after institution of cardiopulmonary bypass from cyanotic Tetralogy of Fallot patients undergoing corrective surgery. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Myocardial samples were collected, immediately after institution of cardiopulmonary bypass from cyanotic Tetralogy of Fallot patients undergoing corrective surgery.
2010-02-27 | E-GEOD-14956 | biostudies-arrayexpress
Project description:To determine cardiac transcription profiles, we collected myocardial samples immediately after institution of cardiopulmonary bypass from acyanotic or cyanotic Tetralogy of Fallot patients undergoing corrective surgery. The transcriptional profile of the mRNA in these samples was measured with gene array technology. Myocardial samples were collected, immediately after institution of cardiopulmonary bypass from acyanotic or cyanotic Tetralogy of Fallot patients undergoing corrective surgery.
2010-02-27 | E-GEOD-14970 | biostudies-arrayexpress
Project description:To determine cardiac transcription profile in cyanotic Tetralogy of Fallot patients subjected to hyperoxic/standard cardiopulmonary bypass, we collected myocardial samples at the end of the ischemic time. The transcriptional profile of the mRNA in these samples was measured with gene array technology Myocardial samples were collected at the end of ischemic time from cyanotic Tetralogy of Fallot patients undergoing corrective surgery using hyperoxic/standard cardiopulmonary bypass
2012-12-06 | E-GEOD-38161 | biostudies-arrayexpress