Single-cell transcriptomic profiling of cardiac CD45+ immune cells 24 hours after ischemia-reperfusion injury in mice with or without splenectomy
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE282100 | GEO | 2025/01/22
REPOSITORIES: GEO
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Project description:Single-cell transcriptomic profiling of cardiac CD45+ immune cells 24 hours after ischemia-reperfusion injury in mice with or without splenectomy
| PRJNA1187192 | ENA
Project description:Lung ischemia-reperfusion (I/R) injury remains one of the common complications after various cardiopulmonary surgeries. I-R injury represents one potentially maladaptive response of the innate immune system which is featured by an exacerbated sterile inflammatory response triggered by tissue damage. Thus, understanding the key components and processes involved in sterile inflammation during lung I-R injury is critical to alter care and extend survival for patients with acute lung injury. We constructed a minipig surgical model of transient unilateral left pulmonary artery occlusion without bronchial involvement to create ventilated lung I-R injury. Lung tissues from minipig with sham operation (one sample), left side lung tissues (the operated side)(one sample) and right side lung tissues (the non-operated side)(one sample) from minipig with lung ischemia-reperfusion were submitted for gene expression array analysis.
2015-12-07 | E-GEOD-75560 | biostudies-arrayexpress
Project description:Our study investigates how the systemic administration of glutamine modulates the transcriptomic profile of neutrophils and renal tubular epithelial cells in the kidney during acute kidney injury.
2021-11-13 | GSE188628 | GEO
Project description:Calcium/calmodulin-dependent protein kinase II (CaMKII) was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. However, the specific functions of the CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury have not been investigated yet. Thus, we studied the roles of the CaMKII isoforms and splice variants in I/R by the use of various CaMKII mutant mice. CaMKIIδC was up-regulated already one day after I/R injury but surprisingly, acute I/R injury was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed nor in conditional CaMKIIδ/γ double-knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction. Leukocyte infiltration was not altered one day but five days after I/R, explaining the late effects of CaMKII deletion on post-I/R remodeling. Other than reported before, we demonstrate that CaMKII is not critically involved in the immediate mechanisms that regulate acute I/R injury but in the process of post-infarct remodeling. We analysed 6 groups in total: 3 groups from wild-type control animals and 3 groups from CaMKII delta/gamma double-KO mice. Sham operated animals served as controls in both wild-type and KO animal groups. 2 different time points in ischia/reperfusion operated animals were investigated: 1 day and 5 days post-surgery.
2014-09-08 | E-GEOD-58486 | biostudies-arrayexpress
Project description:There have been clinical reports of splenectomy as a treatment option for immune-mediated hematologic diseases in humans and dogs. We focused on the efficacy of splenectomy as a treatment for dogs with precursor-targeted immune-mediated anemia. We collected serum samples of pre and post splenectomy in these dogs to investigate the factors that might improve non-regenerative anemia after splenectomy.
2023-02-28 | PXD039913 | JPOST Repository
Project description:Profile the microRNA expression in the Gracilis muscle of rat after 4h ischemia and 24 h reperfusion Following 4 h of ischemia and subsequent reperfusion for 4 h of the gracilis muscles, the specimens were analyzed with an Agilent rat miRNA array to detect the expressed miRNAs in the experimental muscles compared to those from the sham-operated controls. Two-condition experiment, Gracilis muscle after 4h ischemia and reperfusion injury for 24 h v.s. Gracilis muscle (sham control), Biological replicates: 2 control replicates, 2 experiement replicates
2010-04-22 | E-GEOD-21405 | biostudies-arrayexpress
Project description:This study was a part of a larger study assessing the response of young pigs to cardiac ischemia/reperfusion (IR) injury. A mild cardiac injury approach (IR) was used in post-weaned pigs (1-month), to assess regenerative repair in young large mammals after transient ischemic injury. Female and male postnatal day (P)30 pigs were subjected to cardiac ischemia (1-hour) by occlusion of the left anterior descending artery followed by reperfusion (IR), or to sham operation. In pigs subjected to IR, myocardial damage occurred, indicated by increased circulating cardiac troponin I 2-hours post-ischemia. In addition, cardiac ejection fraction (EF) was significantly decreased 2-hours post-ischemia and reduced EF was maintained to the 4-week study end-point. Histology demonstrated evidence of CM cell cycling at 2-months of age in multinucleated CMs in both sham-operated and IR pigs. Following IR, regional scar formation and inflammation in the epicardial region proximal to injury were observed 4-weeks post-IR. Sex differences in cardiac function and collagen deposition were found, highlighting the importance of representing both sexes in cardiac injury studies. Together, our results describe an effective novel cardiac injury model in 1-month old swine, at a time when CM are still cycling. However, pigs subjected to IR show a prolonged decrease in cardiac function, and the formation of a small, regional scar with increased inflammation. Together, these data demonstrate that 1-month old pigs do not regenerate myocardium, but form a scar, after transient IR injury.
2020-04-27 | GSE137293 | GEO
Project description:Splenectomy improves clinical parameters of patients with hereditary spherocytosis but its potential benefit to red blood cell (RBC) morphology and deformability and the mechanism behind remain unknown. We here compared 7 non-splenectomized and 12 splenectomized patients with mutations in the β-spectrin (SPTB) or the ankyrin (ANK1) gene. We showed that hematological parameters, spherocyte abundance, osmotic fragility, intracellular calcium and extracellular vesicle release were largely restored by splenectomy, but cryohemolysis was not. To elucidate the only partial improvement of RBC morphology and deformability by splenectomy, we performed a quantative proteomic analysis and cytoskeleton characterization. Patients exhibited decreased ankyrin and/or β-spectrin contents but the extent of RBC alteration only slightly and negatively correlated with the ankyrin and not with β-spectrin content nor membrane association. In contrast, patients exhibited increased abundance of septins, small GTP-binding cytoskeletal proteins involved in cytokinesis. Among the four septins detected, septins-2,7 and 8 but not 11 were less abundant upon splenectomy and correlated with the disease severity. The septin increase was accompanied by exacerbated oxidative stress especially in the non splenectomized patients. Except cryohemolysis, all the RBC morphology and deformability alterations and oxidative stress correlated with septin content. Impairments can result from RBC maturation defects since endoplasmic reticulum remnants were found in RBCs from non-splenectomized patients and lysosomal and mitochondrial remnants in splenectomised patients. The correlation between septin abundance and disease severity opens the way towards using septins as disease biomarkers. Moreover, the absence of restoration of septin-independent cryohemolysis by splenectomy could question its systematic recommendation
2023-02-13 | PXD034588 | Pride
Project description:In this work, the effect of splenectomy on liver regeneration was studied. For this purpose in 1 series of experiments the animals were reproduced splenectomy, and after 7 days 70% liver resection was performed. It was found that spleen removal leads to a decrease in the migration of Ly6C+ monocytes into the regenerating liver. Using transcriptional analysis it was shown that spleen and peripheral blood monocytes differ in the expression of genes associated with the synthesis of surface receptors necessary for cell migration. The obtained data explain the reason for the preferential migration of spleen monocytes rather than peripheral blood monocytes into the regenerating liver.
2024-04-16 | GSE263764 | GEO
Project description:Ischemia-reperfusion (I/R) injury of the kidney is a major cause of AKI. MicroRNAs (miRs) are powerful regulators of various diseases. We investigated the role of apoptosis-associated miR-24 in renal I/R injury. miR-24 was upregulated in the kidney after I/R injury of mice and in patients after kidney transplantation. Cell-sorting experiments revealed a specific miR-24 enrichment in renal endothelial and tubular epithelial cells after I/R induction. In vitro, anoxia/hypoxia induced an enrichment of miR-24 in endothelial and tubular epithelial cells. Transient overexpression of miR-24 alone induced apoptosis and altered functional parameters in these cells, whereas silencing of miR-24 ameliorated apoptotic responses and rescued functional parameters in hypoxic conditions. miR-24 effects were mediated through regulation of H2A histone family, member X, and heme oxygenase 1, which were experimentally validated as direct miR-24 targets through luciferase reporter assays. In vitro, adenoviral overexpression of miR-24 targets lacking miR-24 binding sites along with miR-24 precursors rescued various functional parameters in endothelial and tubular epithelial cells. In vivo, silencing of miR-24 in mice before I/R injury resulted in a significant improvement in survival and kidney function, a reduction of apoptosis, improved histologic tubular epithelial injury, and less infiltration of inflammatory cells. miR-24 also regulated heme oxygenase 1 and H2A histone family, member X, in vivo. Overall, these results indicate miR-24 promotes renal ischemic injury by stimulating apoptosis in endothelial and tubular epithelial cell. Therefore, miR-24 inhibition may be a promising future therapeutic option in the treatment of patients with ischemic AKI.
| S-EPMC4243358 | biostudies-literature