Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Diabetic lung

ABSTRACT: Effect of type 1 diabetes (induced by streptozotocin 60 mg/kg) on lung gene expression. Wistar rats, male. At age 8 weeks control rats got IP buffer, diabetic rats got streptozotocin. At age 12 weeks animals were anesthetized and lungs removed. RNA was extracted with Trizol, and gene expression array analysis was performed using Affymetrix RAE 230A microarrays according to the directions from the manufacturer. Arrays were scanned using a Hewlett Packard Gene Array scanner, and analyzed with Affymetrix MAS 5.0 software. Expression levels reported are the output from the MAS software. Control rats (n=5) vs diabetic rats (n=7) Each sample is from a different animal (thus these are biological replicates). Samples were NOT pooled. Thus each sample corresponds to one animal.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Erik van Lunteren

PROVIDER: E-GEOD-15900 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Alterations in lung gene expression in streptozotocin-induced diabetic rats.

van Lunteren Erik E Moyer Michelle M Spiegler Sarah S

BMC endocrine disorders 20140115

<h4>Background</h4>Diabetes profoundly affects gene expression in organs such as heart, skeletal muscle, kidney and liver, with areas of perturbation including carbohydrate and lipid metabolism, oxidative stress, and protein ubiquitination. Type 1 diabetes impairs lung function, but whether gene expression alterations in the lung parallel those of other tissue types is largely unexplored.<h4>Methods</h4>Lung from a rat model of diabetes mellitus induced by streptozotocin was subjected to gene ex ...[more]

PMID: 24423257

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Project description:OBJECTIVE: To study the genetic regulatory mechanisms in the remote zone of left ventricular (LV) free wall in order to partly explain the more frequent progression to heart failure after acute myocardial infarction (AMI) in diabetic rats. METHODS: 10 weeks after diabetes mellitus (DM) induction with Streptozotocin (STZ), the left anterior descending coronary arteries of uncontrolled diabetic Sprague-Dawley (SD) rats and non-diabetic ones were ligated without reperfusion. Then, the remote zone tissues of LV free wall were taken as samples at day 1, 7, 14, 28, and 56 post AMI. Significant different expression genes were filterd from Affymetrix Genechip U230 2.0 array by GCOS software. Genetic changes post myocardial infarction were classified by hierarchical clustering of 10 gene chips. And then, the differential expressions of 10 selected transcripts identified by the microarray were examined in greater detail by Real Time-PCR. RESULTS: According to hierarchical clustering, we find that the molecular regulatory expression related to cardiac remodeling in the remote zone to myocardial infarction is quite different as time elapses in both diabetic and non-diabetic rats. The gene expression at day 1 and 7 post AMI in both groups is similar, while the genetic changes at day 14 post AMI in diabetic rats and the ones at day 14 and 28 in non-diabetic rats are classified into the same cluster. And then the genetic changes at day 28 and 56 post AMI in diabetic rats and the ones at day 56 in non-diabetic rats are classified into the same cluster. (Figure.1) The patterns of numerous products of genes expression were used in the cluster, including 118 genes, such as leucine-rich PPR-motif containing (IL-6 signaling pathway), procollagen type I, VI, VIII, and XV, fibronectin1, RT1, and TIMP-1, etc. CONCLUSION: The genetic findings in this study might be the possible mechanism that diabetes mellitus can accerate the progression of post-infarction genetic regulatory expression. Experiment Overall Design: All studies were performed with male SD rats (200-220g), aged 8 weeks, which were obtained from laboratorial animal center of Chinese University of Agriculture. DM was induced with a singleintraperitoneal injection of STZ (65 mg/kg in 0.1mmol/L, pH 4.5 sodium citrate buffer) . Age and body weight matched rats that used as non-diabetic controls were injected with the same dose of sodium citrate buffer (0.1mmol/L, pH 4.5). Ultrastructure changes of myocardium were observed 10 weeks after DM induction by TEM. 10 weeks after DM induction,both diabetic and non-diabetic rats were subjected to left anterior descending coronary artery (LADCA) ischemia for 1-56 days without reperfusion. Two-dimensional echocardiography was utilized to obtain LV dimensions and LV percent fractional shortening at baseline, DM 10weeks, and at 1d, 7d, 14d, 28d, 56d after AMI; the remote zone tissues of LV free wall were taken as samples at day 1, 7, 14, 28, and 56 post AMI for gene chip microarray analysis (10 samples from 30 rats); in addition, heart-to-body weight and heart to tibial length ratios and masson's trichrome staining was measured as an index of cardiac hypertrophy and fibrosis at baseline, DM 10weeks, and at 1d, 7d, 14d, 28d, 56d after AMI.

Project description:Background and Aims: It is well demonstrated that in the beta cell population of the pancreas there is a dynamic turnover, which results from the net balance of several processes; beta cell replication, apoptosis and neogenesis. These processes have been studied in partial pancreatectomy and glucagon-like peptide 1 treated animals, where an increase in pancreas regeneration has been observed. Similarly, sodium tungstate, which decreases hyperglycemia in several animal models of diabetes, promotes a rise in the beta cell mass of nSTZ and STZ animals. However, the molecular mechanisms underlying this pancreas regeneration remain unknown. Therefore the objective of this study is to identify which genes are up or down regulated in the increase of the beta cell population of STZ rats treated with sodium tungstate. Materials and methods: Adult male Wistar (225-250 g) rats were kept under a constant 12-hour light-dark cycle and rats were kept under a constant 12-hour light-dark cycle and were allowed to eat and drink freely. Diabetes was induced by a single i.p. injection of streptozotocin (STZ) (70 mg/Kg body weight) in 0.9% NaCl with 100 mmol/L sodium citrate buffer (pH 4.5). Diabetes was confirmed by determination of its hyperglycaemia (>500mg/dL [Reflotron, Roche Diagnostic]). Healthy rats received an i.p. injection of the vehicle. Treatment started 7 days after the STZ or vehicle injection. Diabetic and healthy rats were divided into two groups. In the first (untreated), rats received deionized drinking water; in the second (treated) group, they were given a solution of sodium tungstate. During the first week of treatment, the rats received a solution of 0.7 mg/mL and in the next 4-5 weeks, the concentration was increased to 2 mg/mL. At the end of the experiment, the animals were sacrificed and pancreatic RNA isolated. Three chips (Affymetrix RAE-230A) were hybridized for each of the four experimental groups (untreated and treated healthy rats and untreated and treated diabetic rats). The raw intensity data obtained from the microarrays was normalized and summarized using the Bioconductor package RMA.

Dataset Information

Diabetic lung

Publications

Alterations in lung gene expression in streptozotocin-induced diabetic rats.

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