Effects of ACTH and DEX on gene expression in rat kidneys
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE6216 | GEO | 2007/11/01
SECONDARY ACCESSION(S): PRJNA97533
REPOSITORIES: GEO
Similar Datasets
Project description:The left kidneys of 8 Sprague-Dawley rats were removed and the rats were left for 2 weeks to recover. After 4 additional days (during which blood pressure measurements were obtained), they were injected daily subcut. with either saline (1ml/kg), adrenocorticotropic hormone (ACTH, 0.2mg/kg) or dexamethasone (DEX, 0.02mg/kg) for 8 days before the right kidney was removed. ACTH and DEX treatment caused hypertension in the rats as illustrated by increased systolic blood pressure. The gene expression patterns of the kidneys were analysed using Affymetrix arrays. Experiment Overall Design: The left kidney of each rat acts as a control for the treated right kidney. Two rats each were treated with either saline, ACTH or DEX.
2008-06-14 | E-GEOD-6216 | biostudies-arrayexpress
Project description:We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively. Sixteen-week-old male Wistar-Kyoto (WKY) and age-matched spontaneously hypertensive rats (SHR) were used. Experiment Overall Design: There were 3 experimental groups: Group 1: 16-week male Wistar-Kyoto rats; Group 2: 16-week male Wistar-Kyoto rats treated with ACTH (0.1mg/kg/day) subcutaneously, for 4 weeks prior to sampling (i.e. during weeks 12-16 of life) ; Group3: 16-week male SHR (spontaneously hypertensive) rats. There were 3 replicate hybridizations in each experimental group. Due to the low yield of total RNA obtained from the arterial sections, each replicate was composed of RNA pooled from 2-3 different rats.
2008-06-15 | E-GEOD-8051 | biostudies-arrayexpress
Project description:We investigated morphometric structure and gene expression by microarray analysis in a small diameter artery, branch of the saphenous artery (a resistance artery), in representative models of renin-angiotensin system (RAS)-dependent and glucocorticoid hypertension, using the spontaneously hypertensive rat (SHR) and adrenocorticotropic hormone (ACTH)-induced hypertensive rat, respectively. Sixteen-week-old male Wistar-Kyoto (WKY) and age-matched spontaneously hypertensive rats (SHR) were used. Keywords: Comparison of global gene expression in resistance arteries of normotensive and genetically hypertensive rats and ACTH-treated rats.
2007-11-28 | GSE8051 | GEO
Project description:We investigated the molecular pathogenesis of LBW rats obtained by intraperitoneal injection of dexamethasone into pregnant animals. Normal-birth-weight (NBW) rats were used as controls with seven animals per group. When the rats were four weeks old, the left kidneys were removed and used for comprehensive label-free proteomic studies
2022-02-15 | PXD018948 | Pride
Project description:SS rats were surgically implanted with a chronic servo-control cuff, the purpose of which is to maintain normal pressure to the left kidney while the right kidney is exposed to high blood pressure. After 7 days of high salt treatment, which induces high blood pressure in the SS rat, rats were anesthetized with pentobarbital, kidneys were flushed and removed. The renal medulla was separated from the cortex using scissors, and the renal medullas were frozen in liquid nitrogen and stored at -80 C.
2017-08-02 | ST000834 | MetabolomicsWorkbench
Project description:Effects of ACTH and DEX on gene expression in rat kidneys
| PRJNA97533 | ENA
Project description:Introduction: Renal ischemia-reperfusion (IR) causes acute kidney injury (AKI) with high mortality and morbidity. The objective of this study was to ameliorate kidney IR injury and identify novel biomarkers for kidney injury and repair. Methods: Left renal ischemia was induced in rats by clamping renal artery for 45 minutes, followed by reperfusion and right nephrectomy. Thirty minutes prior to ischemia, rats (n=8/group) received Valproic Acid (150 mg/kg; VPA), Dexamethasone (3 mg/kg; Dex) or Vehicle (Saline) intraperitoneally. Animals were sacrificed at 3h, 24h or 120h post- IR and blood, urine and kidney were collected. Results: Serum creatinine (mg/dL) at 24 h IR in VPA (2.7±1.8) and Dex (2.3±1.2) was reduced (P<0.05) compared to Vehicle (3.8±0.5). At 3h post-IR, urine albumin (mg/ml) was higher in Vehicle (1.47±0.10), VPA (0.84±0.62) and Dex (1.04±0.73) compared to uninjured/untreated control (0.14±0.26) group. At 24h post-IR urine Lipocalin-2 (µg/ml) was significantly higher (P<0.05) in VPA, Dex and Vehicle groups (9.61-11.36) compared to uninjured/untreated control (0.67±o.29); also, Kidney Injury Molecule-1 (KIM-1; ng/ml) was significantly higher in VPA, Dex and Vehicle groups (13.7-18.7) compared uninjured/untreated control (1.7±1.9). KIM-1 levels were significantly (P<0.05) higher in all groups compared to uninjured/untreated control levels. Histopathology at 3h post IR demonstrated (P<0.05) reduction in ischemic injury in the renal cortex in VPA (Grade 1.6± 1.5) compared to Vehicle (Grade 2.9±1.1) group. Inflammatory cytokines IL1β and IL6 were down-regulated in VPA and Dex groups. BCL2 was higher in VPA group. DNA microarray analysis demonstrated reduced stress response and injury, and improved recovery related gene expression in the kidneys of VPA treated animals. Conclusions: VPA administration reduced kidney IR injury and improved regeneration. KIM-1 and Lipocalin-2 appear to be promising early urine biomarkers of acute ischemic kidney injury. We had three experimental groups. Group A, VPA treatment; Group B, Dexamethasone treatment; and Group C, No treatment (vehicle saline control). Treatments were administered prior to the induction of left renal ischemia. Animals underwent 45 minutes of left renal ischemia, followed by reperfusion, and right nephrectomy as described above. Following reperfusion, animals were sacrificed at 3, 24 or 120 hours (n=8/group). In the 3 hour group, rats were maintained under anesthesia after surgery until sacrifice. In the 24 and 120 hour groups, the rats were recovered and returned to the cages for normal housing. Analgesic buprenorphine (0.05mg/kg) was administered every 12 h for three days post-operatively. After animal sacrifice, urine, blood, and kidney were collected for kidney functional biomarker assays, histology and / or molecular analyses. Urine was obtained via cystocentesis and blood was obtained via the left renal vein. Tissue and urine samples collected from normal (naïve) animals (n=5) were used for baseline measurements. A subset of 46 animals (n = 4-5 per group) were selected for microarray analysis.
2015-07-06 | E-GEOD-58438 | biostudies-arrayexpress
Project description:Introduction: Renal ischemia-reperfusion (IR) causes acute kidney injury (AKI) with high mortality and morbidity. The objective of this study was to ameliorate kidney IR injury and identify novel biomarkers for kidney injury and repair. Methods: Left renal ischemia was induced in rats by clamping renal artery for 45 minutes, followed by reperfusion and right nephrectomy. Thirty minutes prior to ischemia, rats (n=8/group) received Valproic Acid (150 mg/kg; VPA), Dexamethasone (3 mg/kg; Dex) or Vehicle (Saline) intraperitoneally. Animals were sacrificed at 3h, 24h or 120h post- IR and blood, urine and kidney were collected. Results: Serum creatinine (mg/dL) at 24 h IR in VPA (2.7±1.8) and Dex (2.3±1.2) was reduced (P<0.05) compared to Vehicle (3.8±0.5). At 3h post-IR, urine albumin (mg/ml) was higher in Vehicle (1.47±0.10), VPA (0.84±0.62) and Dex (1.04±0.73) compared to uninjured/untreated control (0.14±0.26) group. At 24h post-IR urine Lipocalin-2 (µg/ml) was significantly higher (P<0.05) in VPA, Dex and Vehicle groups (9.61-11.36) compared to uninjured/untreated control (0.67±o.29); also, Kidney Injury Molecule-1 (KIM-1; ng/ml) was significantly higher in VPA, Dex and Vehicle groups (13.7-18.7) compared uninjured/untreated control (1.7±1.9). KIM-1 levels were significantly (P<0.05) higher in all groups compared to uninjured/untreated control levels. Histopathology at 3h post IR demonstrated (P<0.05) reduction in ischemic injury in the renal cortex in VPA (Grade 1.6± 1.5) compared to Vehicle (Grade 2.9±1.1) group. Inflammatory cytokines IL1β and IL6 were down-regulated in VPA and Dex groups. BCL2 was higher in VPA group. DNA microarray analysis demonstrated reduced stress response and injury, and improved recovery related gene expression in the kidneys of VPA treated animals. Conclusions: VPA administration reduced kidney IR injury and improved regeneration. KIM-1 and Lipocalin-2 appear to be promising early urine biomarkers of acute ischemic kidney injury.
2015-07-06 | GSE58438 | GEO
Project description:Investigating a mouse model of Cushing syndrome, synthetic adrenocorticotropic hormone ACTH (Synacthen) was infused for two weeks to markedly increase adrenal mass and plasma corticosterone levels. Gene expression in adrenals was measured to look for changes associated with the adrenal cellular phenotype.
2017-10-11 | E-MTAB-5704 | biostudies-arrayexpress
Project description:We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
2018-11-14 | GSE114031 | GEO