Differential expression profiles of tsRNAs in myocardial ischemic rats with/without caloric restriction
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE158781 | GEO | 2020/10/01
REPOSITORIES: GEO
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Project description:OBJECTIVE: To understand the molecular pathways underlying the cardiac preconditioning effect of short-term caloric restriction (CR). BACKGROUND: Lifelong CR has been suggested to reduce the incidence of cardiovascular disease through a variety of mechanisms. However, prolonged adherence to a CR life-style is difficult. Here we show how short-term CR protects the mouse heart from ischemia. METHODS: Male 10-12 wk old C57bl/6 mice were randomly assigned to an ad libitum (AL) diet with free access to regular chow, or CR, receiving 30% less food over a period of 7 days (d), prior to myocardial infarction (MI) via permanent coronary ligation. Prior to MI (d8), the left ventricles (LV) of AL and CR mice were collected for Western blot, DNA and microRNA (miR) analyses. In separate groups, infarct size, cardiac hemodynamics and protein abundance of caspase 3 was measured at d2 post-MI. RESULTS: This short-term model of CR was associated with cardio-protection, as evidenced by decreased infarct size (18.5±2.4% vs. 26.6±1.7%, N=10/group; P=0.01). cDNA and miR profiles pre-MI (N=5/group) identified genes modulated by short-term CR to be associated with circadian clock, oxidative stress, immune function, apoptosis, metabolism, angiogenesis, cytoskeleton and extracellular matrix (ECM). Western blots pre-MI revealed CR-associated increases in phosphorylated Akt and GSK3ß, reduced levels of phosphorylated AMPK and mitochondrial related proteins PGC-1?, cytochrome C and cyclooxygenase (COX) IV, with no differences in the levels of phosphorylated eNOS or MAPK (ERK1/2; p38). CONCLUSIONS: Short-term CR for only 7d represents a preconditioning strategy that limits infarct size. It is associated with a unique gene and miR signature, including the activation of specific pro-survival kinases. These findings may have implications for therapeutic use of short-term CR. . Male 12 wk-old C57Bl/6 mice were obtained from Charles River (Montreal, PQ, Canada) and maintained for at least 2 weeks before experimentation. Animals were randomly assigned to AL, CR and Lira groups with no initial differences in body weights. AL group mice were allowed ad libitum diet. Lira group mice were injected with Liraglutide (Glucagon-like peptide-1 agonist) at a dose of 200 µg/Kg i.p., twice daily for 7 days which is a mild weight-loss inducing dose and had access to ad libitum food and water. CR group mice were put on a Caloric restriction diet (30% less than normal ad libitum caloric intake) for 7 days to induce weight loss comparable to Lira group mice. Mice for CR and AL were individually caged and their food intake was measured everyday between 10-11 am for 1 week to calculate the average daily food intake. CR mice were fed 30% less than the calculated mean daily AL food consumption. CR cages were inspected daily for any remaining food, and transferred to a new cage every day. For CR group, pre-weighed mouse chow pellets were placed in cages between 10-11 am every day. Body weights were recorded between 10-11 am before and after the 7 day study period. For pre-ischemic assessments, animals (n=5/group/assessment) were sacrificed on day-8 (pre-MI), hearts were immediately extracted, washed in sterile phosphate-buffered saline (PBS), with LV free walls dissected, snap frozen in liquid nitrogen and stored at -80o C.
2015-05-08 | E-GEOD-68646 | biostudies-arrayexpress
Project description:OBJECTIVE: To understand the molecular pathways underlying the cardiac preconditioning effect of short-term caloric restriction (CR). BACKGROUND: Lifelong CR has been suggested to reduce the incidence of cardiovascular disease through a variety of mechanisms. However, prolonged adherence to a CR life-style is difficult. Here we show how short-term CR protects the mouse heart from ischemia. METHODS: Male 10-12 wk old C57bl/6 mice were randomly assigned to an ad libitum (AL) diet with free access to regular chow, or CR, receiving 30% less food over a period of 7 days (d), prior to myocardial infarction (MI) via permanent coronary ligation. Prior to MI (d8), the left ventricles (LV) of AL and CR mice were collected for Western blot, DNA and microRNA (miR) analyses. In separate groups, infarct size, cardiac hemodynamics and protein abundance of caspase 3 was measured at d2 post-MI. RESULTS: This short-term model of CR was associated with cardio-protection, as evidenced by decreased infarct size (18.5±2.4% vs. 26.6±1.7%, N=10/group; P=0.01). cDNA and miR profiles pre-MI (N=5/group) identified genes modulated by short-term CR to be associated with circadian clock, oxidative stress, immune function, apoptosis, metabolism, angiogenesis, cytoskeleton and extracellular matrix (ECM). Western blots pre-MI revealed CR-associated increases in phosphorylated Akt and GSK3ß, reduced levels of phosphorylated AMPK and mitochondrial related proteins PGC-1α, cytochrome C and cyclooxygenase (COX) IV, with no differences in the levels of phosphorylated eNOS or MAPK (ERK1/2; p38). CONCLUSIONS: Short-term CR for only 7d represents a preconditioning strategy that limits infarct size. It is associated with a unique gene and miR signature, including the activation of specific pro-survival kinases. These findings may have implications for therapeutic use of short-term CR. .
2015-05-08 | GSE68646 | GEO
Project description:The molecular mechanism underlying cardiac remodeling following myocardial infarction have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either sham surgery or permanent ligation of the left coronary artery (MI). RNA was isolated from the remote, non-ischemic, regions of the left ventricle. RNA was isolated from 8 sham and 8 MI animals three weeks after surgery. Each group contained 4 males and 4 females. Animals used for the study were 2-3 months old Yorkshire x Landrace swine. Only neutered males entered the study.
2011-12-21 | E-GEOD-27962 | biostudies-arrayexpress
Project description:Male Sprague-Dawley rats were randomly divided into (1) mock surgery (MS) group, mock surgery after EP (EPMS) group, myocardial ischemia (MI) group and MI after EP (EPMI) group. Twenty-four hours after MI or mock surgery , left ventricular tissues below the ligation were collected for the iTRAQ proteomics.
2020-04-23 | PXD017765 | Pride
Project description:In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. We found that AAV9:hYAP significantly improved cardiac function and mouse survival. AAV9:hYAP did not exert its salutary effects by reducing cardiomyocyte apoptosis. Rather, we found that AAV9:hYAP stimulated adult cardiomyocyte proliferation. Gene expression profiling indicated that AAV9:hYAP stimulated cell cycle gene expression, enhanced TGFβ-signaling, and activated of components of the inflammatory response.Cardiac specific YAP activation after MI mitigated myocardial injury after MI, improved cardiac function and mouse survival. These findings suggest that therapeutic activation of hYAP or its downstream targets, potentially through AAV-mediated gene therapy, may be a strategy to improve outcome after MI. Three groups were involved in this study: sham group, AAV9:Luci+MI group and AAV9-YAP+MI group. Each group contained three biological replicates. The sham group had neither myocardial infarction nor AAV injection. The AAV9:Luci +MI(L for brief) group had myocardial infarction and injected with AAV9:Luic. The AAV9:hYAP+MI(YAP for brief) group had myocardial infarction and injected with AAV9:hYAP. 5 days after MI and AAV injection, the heart apexes were collected and the total RNA were isolated for microarray analysis.
2014-05-26 | E-GEOD-54612 | biostudies-arrayexpress
Project description:Prognosis after myocardial infarction (MI) varies greatly depending of the extent of damaged area and the management of biological processes during recovery. Reportedly, the inhibition of the pro-inflammatory S100A9 reduces myocardial damage after MI. We hypothesize that S100A9 blockade induces changes of major signaling pathways implicated in post-MI healing. The S100A9 blocker (ABR-23890) was given for 3 days after coronary ligation. At 3- and 7-days post-MI, ventricle samples were analyzed versus control and sham-operated mice. Blockade of S100A9 modulated the expressed proteins involved in five biological processes: leu-kocyte cell-cell adhesion, regulation of muscle cell apoptotic process, regulation of intrinsic apoptotic signaling pathway, sarcomere organization and cardiac muscle hypertrophy. The blocker induced regulation of 36 proteins interacting with or targeted by the cellular tumor antigen p53, prevented myocardial compensatory hypertrophy, and reduced cardiac markers of post-ischemic stress. The blockade effect was prominent at day 7 post-MI when the quantitative features of ventricle proteome were closer to controls.
2022-05-19 | PXD033683 | Pride
Project description:To investigate the functional significance of myocardial ferritin heavy chain (FtH) in a model of acute myocardial infarction (MI). FtH was deleted using FtH floxed mice and Sm-22 Cre mice on a C57/bl6 background At 3 hours following 45 minutes of ischemia induced via ligation of left ant. decsending coronary artery, ischemic regions were identified, dissected, and total RNA was isolated fand gene expression profiling analysis using data obtained from RNA-seq of 3 different animals. RNA Total RNA isolated from left ventricle under homeostatic (bseline conditions) served as negative ctr. (n=3/group)
2022-07-11 | GSE207609 | GEO
Project description:Immune cell infiltration in response to myocyte death contributes to extracellular matrix (ECM) remodeling and scar formation after myocardial infarction (MI). Caspase-recruitment domain protein 9 (CARD9) which belongs to CARD family acts as an adapter that mediate the transduction of proinflammatory signaling cascades in innate immunity. To investigate the role of CARD9 in cardiac injury and repair post ischemia, we subjected Card9 knockout mice to myocardial infarction (MI) , and then performed RNA-seq and gene expression profiling analysis using the ischemic cardiac tissues at 3 days post-MI, to identify key genes and pathways regulated by CARD9.
2023-10-25 | GSE235257 | GEO
Project description:We established a rat model of myocardial Infarction by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Wistar rats were previously randomly divided into 4 groups: control, ischemia, ischemia-propranolol, and non-ischemia-propranolol. Our data suggested that propranolol could reverse many microRNAs with too high or too low expression in the ischemia group versus control group. Wistar rats were initially anesthetized with pentobarbital (40 mg/kg, i.v.), which were previously randomly divided into 4 groups: control, ischemia (MI), ischemia-propranolol (MI-PRO), and non-ischemia-propranolol (NMI-PRO). The rat model of MI was established by performing a surgical operation of left anterior descending coronary artery occlusion under sterie conditions. Successful occlusion was confirmed by an increase in the amplitude of R wave of lead I during the first few seconds of each occlusion and elevation of S-T segment of lead II, and a 20-30% decline in the arterial blood pressure compared to the pre-ischemic values mesured by a previously installed ECG recorder (BL 420, ChengDu TME Technology Co, Ltd, ChengDu, China). Propranolol was administrated 2 months before the experiment with daily oral doses of 50 mg/kg. Hearts were quickly isolated after the rats were sacrificed and the ischemic zone of the left ventricle was prepared for the miRNA microarray experiment. Control and NMI-PRO animals underwent open chest procedures without coronary artery occlusion.
2010-06-19 | E-GEOD-18129 | biostudies-arrayexpress
Project description:Heart failure (HF) is the most common cause of morbidity and mortality in the developed countries, especially considering the present demographic tendencies in those populations. We identified biologically relevant transcripts that are significantly altered in the early phase of myocardial infarction (MI) and are associated with the development of post-myocardial infarction HF. We collected peripheral blood samples from patients (n=111) with ST-segment elevation myocardial infarction (STEMI) at four time points (admission, discharge, 1 month after MI, and 6 months after MI). Control group comprised patients (n=46) with a stable coronary artery disease and without a history of myocardial infarction. Affymetrix HuGene 1.0 ST arrays were used to analyze mRNA levels in periperal blood mononuclear cells (PBMCs) isolated from the study and control groups. Samples from the first three time points were compared with the samples from the same patients collected 6 months after MI (stable phase) and with the control group. Additionaly, based on plasma NT-proBNP level and left ventricular ejection fraction parameters the STEMI patients were divided into HF and non-HF groups.We attempted to identify transcripts whose differential expression on the 1st day of myocardial infarction predicted which patients would develop symptoms of HF during the 6 months of follow-up. For this purpose, we compared the microarray results for samples collected on admission for the HF group versus the non-HF group.
2015-05-21 | E-GEOD-59867 | biostudies-arrayexpress