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Heart in Diabetes

ABSTRACT: 8 week old rats injected with streptozotocin or buffer alone at age of 8 weeks, heart obtained at 12 weeks (thus animals were diabetic for 4 weeks). Left vent of heart. Keywords: Disease state analysis (diabetes)

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE6880 | GEO | 2008/01/26

SECONDARY ACCESSION(S): PRJNA98555

REPOSITORIES: GEO

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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:We investigated the effects of diabetes, physical training, and their combination on the gene expression of cardiac muscle. Mice were divided to control (C), training (T), streptozotocin-induced diabetic (D), and diabetic training (DT) groups. Training groups performed 1, 3, or 5 weeks of endurance training on a motor-driven treadmill. Muscle samples from T and DT groups together with respective controls were collected 24 hours after the last training session. Gene expression of cardiac muscles were analyzed using Affymetrix Gene chip MG U74Av2 (Affymetrix , Inc., Santa Clara, CA). Experiment was performed on 10 to 15 weeks old male NMRI mice (Harlan, Holland) housed in standard conditions (temperature 22°C, humidity 60 ± 10 %, artificial light from 8.00 am to 8.00 pm, normally 5 animals per cage). Animals had free access to tap water and food pellets (R36, Labfor, Stockholm, Sweden). Animals were randomly divided into healthy and diabetic groups. The diabetic group received a single peritoneal injection of streptozotocin (STZ, Sigma-Aldrich, France, 180 mg/kg) dissolved in sodium citrate buffer solution (0.1 mol/l, pH 4.5) to induce experimental diabetes similar to type 1. The other group received injection of an equal volume of buffer. Diabetes was confirmed 72 hours after the injection by urine glucose testing (Glukotest(r), Roche, Germany), and mice were characterized diabetic when urine glucose values were greater than 200 mg/dl. Diabetic and healthy animals were randomly assigned into 12 groups (n = 5 per group), which were sedentary or trained for one, three or five weeks. Training groups performed 1 hour per day of treadmill running at 21 m/min and 2.5° incline. After one day of familiarization on a rodent treadmill, the mice ran as described above 5 days per week. Mice were sacrificed 24 hours after the last training bout (respective sedentary controls at the same time) by cervical dislocation followed by decapitation. Cardiac muscle was removed, weighed, snap frozen in liquid nitrogen and stored at -80°C for further analysis.

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Heart in Diabetes

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