Cardiopulmonary bypass (CPB) vs sham-operated controls
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE924 | GEO | 2003/12/20
SECONDARY ACCESSION(S): PRJNA87947
REPOSITORIES: GEO
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Project description:heart from rats exposed to cardiopulmonary bypass (CPB) vs sham-operated controls
2010-05-27 | E-GEOD-924 | biostudies-arrayexpress
Project description:hearts from rats exposed to cardiopulmonary bypass (CPB) vs sham-operated controls Keywords = rat Keywords = heart Keywords = cytokine Keywords = inflammation Keywords: repeat sample
2003-12-20 | GSE922 | GEO
Project description:heart from rats exposed to cardiopulmonary bypass (CPB) vs sham-operated controls Keywords = rat Keywords = cardiac Keywords = cytokine Keywords = inflammation Keywords: repeat sample
2003-12-20 | GSE921 | GEO
Project description:Cardiopulmonary bypass (CPB) vs sham-operated controls
| PRJNA87947 | ENA
Project description:Acute kidney Injury (AKI) following open-heart surgery with cardiopulmonary bypass (CPB) is associated with an increased morbidity and mortality. The goal of this study is to explore patterns of gene expression in human AKI following CPB. This prospective observational study was approved by the Institutional Review Board Human Subjects Committee. Design and methods: Peripheral blood RNA samples were collected prospectively from a cohort of 30 patients at Caritas St. Elizabeths Medical Center in Boston, MA, undergoing CPB at time points immediately prior, and two and 24 hours following CPB. Gene expression patterns of four patients who developed AKI (cases) following CPB will be compared with six patients matched for clinical characteristics, who did not develop AKI (controls). AKI was defined by an incremental increase in serum creatinine of 30% within 72 hours following CPB. For peripheral blood RNA sampling, 2.5 ml of venous whole blood was collected into PAXgene Blood RNA Tube collection tubes (PreAnalytiX GmbH, Hombrechtikon, CH). Whole blood RNA was extracted with the PAXgene Blood RNA extraction Kit according to the manufacturers instructions (PAXgene RNA Kit Handbook, 06/2005). All biological samples are stored at 80° C.
2009-12-12 | E-TABM-595 | biostudies-arrayexpress
Project description:Objectives: Systemic inflammatory response syndrome (SIRS) is a frequent complication of cardiopulmonary bypass (CPB). SIRS is associated with significant morbidity and mortality, but its pathogenesis remains incompletely understood, and as a result biomarkers are lacking, and treatment remains expectant and supportive. This study aimed to understand the pathophysiological mechanisms driving SIRS induced by CPB and identify novel therapeutic targets that might reduce systemic inflammation and improve patient outcomes. Methods: 21 patients undergoing cardiac surgery and CPB were recruited, and blood was sampled before, during and after surgery. SIRS was defined using the American College of Chest Physicians/Society of Critical Care Medicine criteria. We performed immune cell profiling, whole blood transcriptomics and measured individual mediators in plasma/serum to characterise SIRS induced by CPB. Results: Nineteen patients fulfilled criteria for SIRS, with a mean duration of 2.7 days. Neutrophil numbers rose rapidly with CPB and remained elevated for at least 48 hours afterwards. Transcriptional signatures associated with neutrophil activation and degranulation were enriched during CPB. We identified a network of cytokines governing these transcriptional changes, including granulocyte colony stimulating factor (G-CSF), a regulator of neutrophil production and function. Conclusions: We identified neutrophils and G-CSF as major regulators of CPB induced systemic inflammation. Short-term targeting of G-CSF could provide a novel therapeutic strategy to limit neutrophil mediated inflammation and tissue damage in SIRS induced by CPB.
2024-02-28 | GSE253782 | GEO
Project description:Cardiopulmonary bypass (CPB), the mechanical support required during the majority of cardiac surgeries, causes significant systemic inflammation and multi-organ dysfunction that is especially severe in neonatal patients. Currently, the limited understanding of the molecular mechanisms that underlie CPB-associated inflammation presents a significant barrier to the development of therapeutic interventions. To address this knowledge gap, we performed mRNA sequencing of total circulating leukocytes from neonatal patients undergoing CPB. The transcriptional signatures across 7 time points ranging from pre-CPB, during CPB, to 24 hours post-CPB were found to be dominated by myeloid cells, particularly monocytes. INTERLEUKIN-8 (IL8) and TUMOR NECROSIS FACTOR-α (TNFα) were two inflammatory cytokines specifically and robustly upregulated in the leukocytes from both CPB patients and piglets exposed to CPB. To delineate the mechanism how CPB activates cytokine production, we exposed THP-1 cells, a human monocyte cell line, in vitro to CPB-like conditions including artificial surfaces, high shear stress and cooling/rewarming. The in vitro CPB data recapitulated the in vivo CPB condition in that IL8 and TNFα were strongly upregulated. Shear stress was the major driver of cytokine expression as compared to the temperature or plastic exposure. Extracellular calcium influx was found essential for the shear-stress mediated upregulation of cytokines via the MEK/ERK/AP-1 and Calcineurin/NFAT pathways. After being exposed to CPB conditions, a subpopulation of THP-1 cells died by apoptosis and TNFα-mediated necroptosis, the latter form of which potentially contribute to the post-CPB tissue injuries. Together, our study is the first to elucidate the shear-stress modulated molecular mechanisms leading to systemic inflammation in pediatric CPB and the link between inflammation and organ damage. Calcium signaling pathways and TNFα signaling are novel targets for therapeutic development to improve clinical outcomes. To our knowledge, these are also the first data to implicate necroptosis in CPB and show that shear stress can activate necroptosis.
2020-12-06 | GSE143780 | GEO
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
Project description:To determine cardiac transcription profile in cyanotic Tetralogy of Fallot patients subjected to conrolled reoxygenation 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 conrolled reoxygenation cardiopulmonary bypass
2012-12-06 | E-GEOD-38162 | biostudies-arrayexpress
Project description:Tetralogy of Fallot (ToF) and Atrial Septal Defects (ASD) are the most common types of congenital heart disease and a major cause of childhood morbidity and mortality. Cardiopulmonary bypass (CPB) is used during corrective cardiac surgery to support circulation and heart stabilization. However, this technique triggers systemic inflammatory and stress response and consequent increased risk of postoperative complications. The aim of this study was to define the molecular bases of ToF and ASD pathogenesis and response to CPB and identify new specific biomarkers. We conducted comparative transcriptome analysis of right atrial biopsies from 10 ToF and 10 ASD patients before (Pre-CPB) and after (Post-CPB) surgery. Pre-CPB samples showed significant differential expression of 72 genes (DEGs), 28 of which were overexpressed in ToF and 44 in ASD. According to Gene Ontology annotation, the mostly enriched biological processes were represented by matrix organization and cell adhesion in ToF and by muscle development and contractility in ASD specimens. GSEA highlighted the specific enrichment of known hypoxia gene sets in ToF samples, pointing to a role for hypoxia in disease pathogenesis. The post-CPB myocardium exhibited significant alterations in the expression profile of genes related to transcription regulation, growth/apoptosis, inflammation, cell adhesion/matrix organization, and oxidative stress. Among DEGs, only 70 were common to the two disease groups, whereas 110 and 24 were unique in ToF and ASD, respectively. Interestingly, gene expression changes in ASD samples followed a consensus hypoxia profile. These data define ToF- and ASD-specific myocardial transcriptional signatures and demonstrate differential gene reprogramming in response to CPB in the two pathologies, with potential prognostic and therapeutic implications.
2020-01-21 | GSE132176 | GEO