Expression data from mouse kidney intraperitoneally administered with LPS and Stx
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PROVIDER: PRJNA748385 | ENA |
REPOSITORIES: ENA
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Project description:Mice intraperitoneally administered with LPS and Stx exhibit HUS-like pathology. While mouse and human Gb3 localization is different, LPS and Stx induced kidney injury models in mice have been used to confirm responsiveness to various stx-related inflammatory pathways and treatments. In order for this mouse model to apply tHUS in humans, more detailed and exhaustive comprehension of this animal model is needed. Although molecular studies have been conducted on this mouse model before, we consider that there is still scope for further investigation of molecular pathways and studies on kidney damage segments. Overall, Biological pathways, upstream regulators, and downstream biological activities occurring in the kidney after LPS/Stx administration were identified through Ingenuity Pathway Analysis ™ using the result of microarray. In addition, we identified the detailed damaged site in the renal tubule from the down-regulation gene revealed by microarray.
2021-09-01 | GSE180476 | GEO
Project description:miRNome changes in the mouse kidney, LPS-administered vs. control
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Project description:Comparing control and LPS-administered with either 40 mg/kg LPS for early time points (ETP) or 10 mg/kg for late time points (LTP). In ETP, 7-7 animals were sacrificed at 1.5 and at 6 hours after LPS administration. In LTP, 7-7 animals were sacrificed at 24 and 48 hours after the endotoxin injection. In both ETP and LTP 7 mice were received equal volume of saline to use as negative control. Four animals were selected for miRNA microArray analysis based on their proinflammatory (TNF-α and IL-6) mRNA expression levels.
2019-11-06 | GSE139919 | GEO
Project description:To investigate the transcriptional changes caused by Stx1 and Stx2 in human kidney microvascular cells (HKMECs), and the effects of GCSi pre-treatment on Stx-mediated effects
2024-01-24 | GSE205723 | GEO
Project description:Microarray analyses provide a powerful approach to identify gene expression alterations following kidney transplantation. However, the heterogeneity of human kidney transplant specimens and the variation in sample preparation precludes conclusions regarding the underlying mechanisms of the observed alterations. We used a well defined experimental rat kidney transplantation model with consistent transplant and sample preparation procedures to analyze genome wide changes in gene expression after syngeneic (sTX) and allogeneic transplantation (aTX) four days after transplantation. Both interventions were associated with dramatic changes in gene expression. Genes and Pathways related to immune response were extremely up regulated after aTX. Several of the up regulated genes have been described by other groups and we are able to proof this in one study. But several genes are reported for the first time to be up regulated in expression after renal aTX. The function of these genes in acute rejection process has to be evaluated. On the other hand the up regulation of regulatory or protective genes indicates that regulatory mechanism are activated after aTX trying to down regulate the immune response or protect the tissue against the immune system. The study is capable to serve as a representative study in aTX mediated gene expression by covering the known transcriptional changes reported by other groups and identification of novel markers and pathways. Further analysis of the duplicated datasets by other groups can help for a better understanding of the mechanisms mediated by acute rejection and thereby increase the therapeutic threatment. Experiment Overall Design: Male LewisâBrown-Norway (LBN) and Lewis (LEW) rats were used in the present study. All recipients were bilaterally nephrectomized immediately before donor kidney TX. In brief, the left kidney including ureter, renal artery, a piece of aorta and renal vein was transplanted into the recipient. For the allogeneic TX (aTX) model, kidneys of LBN-rats (n=5) were transplanted into LEW-rats and for the syngeneic TX (sTX) model kidneys from LBN-rats (n=5) were transplanted into LBN-rats. The LBN-into-Lewis model leads to marked histological changes typical for acute transplant rejection. The second kidney of the LBN-donors (n=5) served as controls.
2008-06-14 | E-GEOD-6497 | biostudies-arrayexpress
Project description:The Escherichia coli strain Nissle 1917 (EcN) is used as a probiotic for the treatment of certain gastrointestinal diseases in several European and non-European countries. In vitro studies showed EcN to efficiently inhibit the production of Shiga toxin (Stx) by Stx producing E. coli (STEC) such as Enterohemorrhagic E. coli (EHEC). The occurrence of the latest EHEC serotype (O104:H4) responsible for the great outbreak in 2011 in Germany was due to the infection of an enteroaggregative E. coli by a Stx 2-encoding lambdoid phage turning this E. coli into a lysogenic and subsequently into a Stx producing strain. Since EHEC infected persons are not recommended to be treated with antibiotics, EcN might be an alternative medication. However, because a harmless E. coli strain might be converted into a Stx-producer after becoming host to a stx encoding prophage, we tested EcN for stx-phage genome integration. Our experiments revealed the resistance of EcN towards not only stx-phages but also against the lambda phage. This resistance was not based on the lack of or by mutated phage receptors. Rather the expression of certain genes (superinfection exclusion B (sieB) and a phage repressor (pr) gene) of a defective prophage of EcN was involved in the complete resistance of EcN to infection by the stx- and lambda phage. Obviously, EcN cannot be turned into a Stx producer. Furthermore, we observed EcN to inactivate phages and thereby to protect E. coli K-12 strains against infection by stx- as well as lambda-phages. Inactivation of lambda-phages was due to binding of lambda-phages to LamB of EcN whereas inactivation of stx-phages was caused by a thermostable protein of EcN. These properties together with its ability to inhibit Stx production make EcN a good candidate for the prevention of illness caused by EHEC and probably for the treatment of already infected people.
2018-06-14 | GSE109932 | GEO
Project description:The aim of this study was to identify miRNAs that regulate AKI and develop their applications as diagnostic biomarkers and therapeutic agents. First, kidney tissues from two different AKI mouse models, namely, AKI induced by the administration of lipopolysaccharide (LPS) causing sepsis (LPS-AKI mice) and AKI induced by renal ischemia–reperfusion injury (IRI-AKI mice), were exhaustively screened for their changes of miRNA expression compared with that of control mice by microarray analysis.
2021-05-14 | GSE172038 | GEO
Project description:Microarray analyses provide a powerful approach to identify gene expression alterations following kidney transplantation. However, the heterogeneity of human kidney transplant specimens and the variation in sample preparation precludes conclusions regarding the underlying mechanisms of the observed alterations. We used a well defined experimental rat kidney transplantation model with consistent transplant and sample preparation procedures to analyze genome wide changes in gene expression after syngeneic (sTX) and allogeneic transplantation (aTX) four days after transplantation. Both interventions were associated with dramatic changes in gene expression. Genes and Pathways related to immune response were extremely up regulated after aTX. Several of the up regulated genes have been described by other groups and we are able to proof this in one study. But several genes are reported for the first time to be up regulated in expression after renal aTX. The function of these genes in acute rejection process has to be evaluated. On the other hand the up regulation of regulatory or protective genes indicates that regulatory mechanism are activated after aTX trying to down regulate the immune response or protect the tissue against the immune system. The study is capable to serve as a representative study in aTX mediated gene expression by covering the known transcriptional changes reported by other groups and identification of novel markers and pathways. Further analysis of the duplicated datasets by other groups can help for a better understanding of the mechanisms mediated by acute rejection and thereby increase the therapeutic threatment. Keywords: gene expression changes due to acute rejection
2007-04-01 | GSE6497 | GEO