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7-Hydroxycoumarin attenuates colistin-induced kidney injury in mice through the inhibition of HDAC1 and the activation of Nrf2 signaling

ABSTRACT: RNA sequencing of kidney tissues was performed to investigate the mechanism of 7-Hydroxycoumarin attenuates colistin-induced kidney injury in mice

ORGANISM(S): Mus musculus

PROVIDER: GSE150518 | GEO | 2020/05/14

REPOSITORIES: GEO

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7-Hydroxycoumarin attenuates colistin-induced kidney injury in mice through the inhibition of HDAC1 and the activation of Nrf2 signaling

Project description:7-Hydroxycoumarin attenuates colistin-induced kidney injury in mice through the inhibition of HDAC1 and the activation of Nrf2 signaling

| PRJNA632626 | ENA

Differential gene expression in mouse kidney following 72 hours of colistin exposure by Illumina WG-6_V2 array

2013-11-05 | GSE46410 | GEO

Differential gene expression in mouse kidney following 72 hours of colistin exposure by Illumina WG-6_V2 array

Project description:Colistin sulfate (polymixin E) is an antibiotic prescribed with resurging frequency for multidrug resistant gram negative bacterial infections. It is associated with nephrotoxicity in humans in up to 33% of cases. Little is known regarding genes involved in colistin nephrotoxicity. A murine model of colistin-mediated kidney injury was developed. C57/BL6 mice were administered saline or colistin at a dose of 16mg/kg/day in 2 divided doses. An Illumina gene expression array was performed on kidney RNA harvested 72 hours after first colistin dose to identify differentially expressed genes early in drug treatment. Array platform was MouseWG-6, 48,000 probes. Drug given intraperitoneal. Total RNA was isolated from mouse kidneys which were harvested upon sacrifice. 12 total 10 week old C57 bl6 mice were analyzed. Six mice were administered 0.1% saline twice daily, six mice were given colistin at 16 mg/kg/day in 2 divided doses. The 2 groups were randomized to 2 different MouseWG-6_V2_0_R2_11278593 and groups were compared.

2013-11-05 | E-GEOD-46410 | biostudies-arrayexpress

Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Acute kidney injury (AKI) represents a common complication in critically ill patients that is associated with an increased morbidity and mortality. Currently, no effective treatment options are available. Here, we show that glutamine significantly attenuates leukocyte recruitment and inflammatory signaling in human and murine tubular epithelial cells (TECs). In a murine AKI model induced by ischemia-reperfusion-injury (IRI) we show that glutamine causes transcriptomic and proteomic reprogramming in renal TECs and neutrophils, resulting in decreased epithelial apoptosis, neutrophil recruitment and improved mitochondrial functionality and respiration provoked by an ameliorated oxidative phosphorylation. We identify the proteins glutamine gamma glutamyltransferase 2 (Tgm2) and apoptosis signal-regulating kinase (Ask1) as the major targets of glutamine in apoptotic signaling. Increased Tgm2 expression and reduced Ask1 activation result in decreased JNK activation leading to a diminished mitochondrial intrinsic apoptosis in kidneys upon IRI-induced AKI and under hypoxia or following TNFα-treatment of TECs. Consequently, glutamine administration attenuated kidney injury in vivo during AKI progression as well as TEC viability in vitro under inflammatory and hypoxic conditions.

2023-03-11 | PXD029723 | Pride

Colistin resistant A. baumannii: genomic and transcriptomic traits acquired under colistin therapy

Project description:Comparative Genomic and Transcriptomic Characterization of Colistin-Resistant Acinetobacter baumannii

2019-01-23 | GSE109951 | GEO

Aminocandin versus Aminocandin plus Colistin

Project description:We found that the antibiotic colistin acts synergistically with antifungals of the echinocandin class (e.g. aminocandin) on C. albicans cells. In order to elucidate the mode of action of colistin in fungi we performed microarray analysis of samples treated with only aminocandin (0.00125µg/ml) or treated with aminocandin (0.00125µg/ml) and colistin (5µg/ml). We compared: (A). untreated cells to cells treated with aminocandin only; (B). cells treated with aminocandin to cells treated with aminocandin and colistin (which is the focus of this experiment). By comparing those datasets it should be possible to identify genes differentially expressed in response to aminocandin and in response to both drugs. And subsequently to be able to interpret where in the cell colistin acts. (See related experiment in ArrayExpress: E-MEXP-3437 for comparison between untreated cells vs cells treated with aminocandin only.)

2012-03-03 | E-MEXP-3438 | biostudies-arrayexpress

Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

Project description:Glutamine attenuates renal ischemia-reperfusion injury and prevents acute kidney damage

| PRJNA779717 | ENA

Expression data from the kidney of Sprague-Dawley rats given colistin methanesulfonate sodium

Project description:To investigate the mechanism of nephrotoxicity, colistin methanesulfonate sodium (CMS; 25 or 50 mg/kg) was administered via intraperitoneal injection to Sprague–Dawley rats daily over 7 d. Affymetrix GeneChip microarrays indicated 894 differentially expressed genes in groups treated with CMS (ANOVA, FDR < 0.05, fold change ≥ 1.3).

2018-10-26 | GSE121792 | GEO

Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice

Project description:Inhibition of microbiota-dependent TMAO production attenuates chronic kidney disease in mice

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Podocyte-specific induction of Krüppel-like factor 15 restores differentiation markers and attenuates kidney injury in proteinuric kidney disease

Project description:Podocyte injury is the hallmark of proteinuric kidney diseases, such as Focal Segmental Glomerulosclerosis and Minimal Change Disease. Therapeutic strategies in the management of proteinuric diseases are limited. Although agents such as glucocorticoids, cyclosporine, and rituximab have direct effects on the podocyte by stabilizing its actin cytoskeleton, these drugs are riddled with systemic toxicity and off-target effects that hinder their chronic use. We previously demonstrated that the loss of the kidney-enriched zinc finger transcription factor, Krüppel-like factor 15 (KLF15), increases susceptibility to proteinuric kidney disease as well as attenuates the salutary effects of retinoic acid and glucocorticoids in the podocyte. Here, we show that podocyte-specific induction of KLF15, using the tetracycline-inducible system, attenuated podocyte injury, glomerulosclerosis, tubulointerstitial fibrosis and inflammation, while improving renal function and overall survival in HIV-1 transgenic mice. Enrichment analysis of mRNA sequencing of isolated glomerular extracts from this model shows that podocyte-specific induction of KLF15 activates pathways involved in stabilization of actin cytoskeleton, focal adhesion, and podocyte differentiation. Transcription factor enrichment analysis, with further experimental validation, suggests that KLF15 activity is in part mediated by Wilms Tumor 1 (WT1), a transcription factor known to be critical for podocyte differentiation. Further, we confirmed the benefits of podocyte-specific induction of KLF15 in the adriamycin-induced proteinuric murine model. Collectively, these observations suggest that induction of KLF15 might be a potential therapeutic target in the treatment of proteinuric kidney disease.

2018-08-02 | GSE117987 | GEO

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