RNA-seq of islet, FACS- sorted CD45+Ly6C-CD11B+CD11C+F4/80+ cells from C57bl6/J male mice that were treated with low dose streptozotocin (STZ) or acetate buffer
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ABSTRACT:
PROVIDER: PRJEB28777 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2811700_1.fastq.gz | Fastqsanger.gz | |||
| ERR2811700_2.fastq.gz | Fastqsanger.gz | |||
| ERR2811710_1.fastq.gz | Fastqsanger.gz | |||
| ERR2811710_2.fastq.gz | Fastqsanger.gz | |||
| ERR2811691_1.fastq.gz | Fastqsanger.gz |
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Project description:The experiment was designed to obtain a broader unbiased view of the changes in islet macrophages following low dose STZ challenge. Mice were purchased from Jackson Laboratory (Bar Harbor, ME). 16-20-week-old C57BL/6J males were given 30 mg/kg STZ or acetate buffer (control) i.p. (intraperitoneal injection) for 5 consecutive days. Following the first STZ or buffer injection mice were sacrificed on day 14 and islets were isolated by collagenase digestion. Freshly isolated islets were dispersed in 0.02% Trypsin-EDTA for 3 minutes followed by up to 1 minute of pipetting under a stereomicroscope to obtain a single cell solution. Islet media was added to stop the reaction. Islets from 10 mice were pooled per sample (N). Dispersed islets were washed with FACS buffer (1% heat inactivated FBS, 1 mM EDTA, 11 mM glucose in PBS). Cells were kept on ice and pre-incubated with Fc Block (1:100) for 5 minutes, followed by 30 min incubation with CD45-eFluor 450 (1:250; clone 30-F11), Ly-6C-APC (1:1,200; clone HK1.4), CD11b-PE (1:1,200; clone M1/700, F4/80-FITC (1:150; clone BM8), CD11c-PECy7 (1:150; clone N418), and the viability dye 7AAD (1:2,000). Unstained, single stains, and fluorescence minus one controls were used for setting gates and compensation. Viable, single CD45+Ly6c-Cd11b+Cd11c+F4/80+ cells were sorted using a BD FACS Aria IIu directly into lysis buffer, and the RNeasy Plus Micro Kit from Qiagen was used to isolate total RNA. Total RNA quality control quantification was performed using an Agilent 2100 Bioanalyzer. All RNA samples had an RNA integrity number (RIN) ≥9.1. The NeoPrep Library Prep System from Ilumina was used for library preparation followed by sequencing using standard Illumina methods and Ilumina NextSeq500.
2019-11-01 | E-MTAB-7234 | biostudies-arrayexpress
Project description:RNA-seq of islet, FACS- sorted CD45+Ly6C-CD11B+CD11C+F4/80+ cells from C57bl6/J male mice that were treated with low dose streptozotocin (STZ) or acetate buffer
2018-11-12 | E-MTAB-7234 | ExpressionAtlas
Project description:8 week old rats injected with streptozotocin or buffer alone at age of 8 weeks, diaphragm muscle obtained at age of 12 weeks (thus animals were diabetic for 4 weeks) Experiment Overall Design: Three control rats (normal diaphragm #1, 2, 3) Experiment Overall Design: Three diabetic rats (diabetic diaphragm #1, 2, 3)
2009-11-28 | E-GEOD-4653 | biostudies-arrayexpress
Project description:Low protein (LP) during gestation leads to low birth weight and poor fetal growth, with altered islet development and glucose intolerance in adulthood. Additionally, LP offspring fail to regenerate their β-cells following depletion with streptozotocin (STZ), in contrast to control-fed offspring that are capable of β-cell regeneration. Our objective was to identify genes and signalling pathways that may be critically altered in LP offspring rendering them susceptible to develop long term glucose intolerance and decreased β-cell plasticity. Pregnant Balb/C mice were place on a control (20% protein) or isocaloric low protein (8%) diet for the period of gestation, and then all dams were switch to the control diet at birth. Female offspring were injected with streptozotocin (35 mg/kg body weight; sodium citrate buffer 0.1 mol/L, pH 4.5) or vehicle (sham). Total RNA was extracted from pancreas of 30 day old female offspring (n=3) and hybridized to Affymetrix GeneChips.
2013-06-01 | E-GEOD-38215 | biostudies-arrayexpress
Project description:Bezafibrate (BEZ), a pan activator of peroxisome proliferator-activated receptors (PPARs), is generally used to treat hyperlipidemia. Clinical trials on patients suffering from type 2 diabetes indicated that BEZ also has beneficial effects on glucose metabolism, but the underlying mechanisms remain elusive. Much less is known about the function of BEZ in type 1 diabetes. Here, we show that BEZ treatment markedly improves hyperglycemia, glucose and insulin tolerance in streptozotocin (STZ)-treated mice, an insulin-deficient mouse model of type 1 diabetes presenting with very high blood glucose levels. Furthermore, BEZ-treated mice also exhibited improved metabolic flexibility as well as an enhanced mitochondrial mass and function in the liver. Our data demonstrate a beneficial effect of BEZ treatment on STZ mice reducing diabetes and suggest that BEZ ameliorates impaired glucose metabolism possibly via augmented hepatic mitochondrial performance, improved insulin sensitivity and metabolic flexibility. We performed gene expression microarray analysis on liver tissue derived from streptozotocin-treated mice treated with bezafibrate in addition.
2016-06-29 | E-GEOD-79008 | biostudies-arrayexpress
Project description:Phloridzin is a dihydrochalcone typically contained in apples. A diet containing 0.5 % phloridzin significantly improves hyperglycemia but not hypoinsulinemia and tissue lipid peroxidation in streptozotocin (STZ)-induced diabetic mice after 14 days. The phloridzin diet has no effect on the alteration of hepatic gene expression in STZ-induced diabetic mice. A quantitative RT-PCR analysis showed a reversal of the STZ induction of the sodium/glucose cotransporter gene Sglt1 and the drug-metabolizing enzyme genes Cyp2b10 and Ephx1 in the small intestine of mice fed a 0.5% phloridzin diet. These mice also showed a reversal of the STZ-mediated renal induction of the glucose-regulated facilitated glucose transporter gene Glut2. Dietary phloridzin improved the abnormal elevations in blood glucose level and the overexpression of Sglt1, Cyp2b10 and Ephx1 in the small intestine of STZ-induced diabetic mice.
2012-05-30 | GSE38138 | GEO
Project description:Streptozotocin (STZ) is an anti-cancer drug that is primarily used to treat neuroendocrine tumors (NETs) in clinical settings and develop type 1 diabetes rodent models in experimental fields. STZ is incorporated into cells through the glucose transporter, GLUT2, which is primarily expressed in pancreatic β-cells or proximal tubular epithelial cells in the kidney. However, its cytotoxic effects on kidney cells have been underestimated and the underlying mechanisms remain unclear. We herein demonstrated that DNA damage and subsequent p53 signaling were responsible for the development of STZ-induced tubular epithelial injury. We detected tubular epithelial DNA damage in NET patients treated with STZ. Unbiased transcriptomics of tubular epithelial cells in vitro showed the activation of the p53 signaling pathway by STZ. STZ induced DNA damage and activated p53 signaling in vivo in a dose-dependent manner, resulting in reduced membrane transport. The localization of STZ-induced kidney injury was limited to within the kidney cortex, which was independent of blood glucose. The pharmacological inhibition of p53 and sodium-glucose transporter 2 (SGLT2) mitigated STZ-induced epithelial injury. However, the cytotoxic effects of STZ on pancreatic β-cells were preserved in SGLT2 inhibitor-treated mice. The present results demonstrate the strong proximal tubular-specific cytotoxicity of STZ and the underlying mechanisms in vivo, which may be ameliorated by a SGLT2 inhibitor pretreatment. Since the cytotoxic effects of STZ against β-cells were not impaired by dapagliflozin, a pretreatment with a SGLT2 inhibitor has potential as a preventative remedy for kidney injury in NET patients treated with STZ.
2023-06-07 | GSE215337 | GEO
Project description:Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)-induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes-associated liver injury. We fed STZ-induced diabetic mice with diets containing 0.1% or 0.5% quercetin for 2 weeks and compared the patterns of hepatic gene expression in these groups of mice using a DNA microarray. Diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a).
2012-05-23 | GSE38067 | GEO
Project description:Chemicals, such as MNU (N-methyl-N-nitrosourea) and NaIO3 (sodium iodate), are widely used to induce retinal degeneration in rodents. Streptozotocin (STZ) is an analog of N-acetyl glucosamine in which an MNU moiety is linked to a hexose and has a special toxic effect on insulin-producing pancreatic β-cells. It is commonly used to induce hyperglycemia to model diabetes. While intracerebroventricular injection of STZ can produce Alzheimer's disease independent of hyperglycemia, most retinal studies using STZ focus on the effects of hyperglycemia on the retina, but whether STZ has any impact on retinal cells independent of hyperglycemia is unknown. We aimed to investigate the role of cytotoxicity of STZ in rat retina. Intravitreal (5ug or 10ug) or subcutaneous (30mg/kg) injection of STZ at the early stage of newborn rats couldn’t induce hyperglycemia but caused NSIR (neonatal STZ-induced retinopathy), including reduced ERG amplitudes, retinal rosettes and apoptosis, cell cycle arrest, microglial activation, and delayed retinal angiogenesis. STZ did not affect the early-born retinal cell types but significantly reduced the late-born ones. Short-term and long-term hyperglycemia had no significant effects on the NSIR phenotypes. RNA sequencing revealed that STZ induces oxidative stress and activates the p53 pathway of retinal cells. Locally or systemically, STZ injection after P8 couldn’t induce NSIR when all retinal progenitors exit the cell cycle. Thus, NSIR in rats is independent of hyperglycemia but due to STZ’s direct cytotoxic effects on retinal progenitor cells. NSIR is a typical reaction to STZ-induced retinal oxidative stress and DNA damage. This significant finding suggests that NSIR may be a valuable model for studying retinal progenitor DNA damage-related diseases, potentially leading to new insights and treatments.
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Project description:Staphylococcus aureus is an important human pathogen causing skin infection and many serious diseases such as pneumonia, sepsis, and toxic shock syndrome. We identified two anti-cancer drugs, streptozotocin (STZ) and floxuridine (FU), as promising lead compounds for further optimization into effective anti-virulence drugs against S. aureus infections. To understand the molecular mechanism of the in vivo efficacy of STZ and FU, we carried out RNA-seq. S. aureus USA300 was treated with 1 ug/mL (= 3.8 uM for STZ, 4 uM for FU) for 3 h. STZ treatment altered transcription of 829 genes (382 up-regulated; 447 down-regulated) whereas FU affected the transcription of 1192 genes (580 up-regulated; 612 down-regulated). Importantly, both compounds inhibited the transcription of the other virulence-regulatory systems such as Agr, Arl, and SarA. Therefore, the results indicate that the high in vivo efficacy of STZ and FU might be due to their repression of multiple virulence regulatory systems.
2018-02-13 | GSE104069 | GEO