Activation of NOTCH and BMP signaling pathways during acute hypoxic stress in cardiac mesenchymal cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE201888 | GEO | 2022/05/02
REPOSITORIES: GEO
Similar Datasets
Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs) Myocardial infarction (MI) was induced in male Wistar rats by ligation of the proximal left coronary artery. The sham-operated group (control group) was subjected to the same protocol, except that the suture was not tied around the proximal left coronary artery. Sham-operated rats (n=6) and rats with small (n=6), moderate (n=6), and large (n=5) MI size were included into the experiment two months after the operation. Then, left ventricules and blood samples were obtained for RNA extraction and hybridization on Affymetrix microarrays. Microarrays were used to compare the LV and PBMCs transcriptomes of control and experimental animals. The development of heart failure was estimated by echocardiography and catheterization.
2013-11-15 | E-GEOD-47495 | biostudies-arrayexpress
Project description:We conducted a global quantitative phosphoproteomic and proteomic analysis of left ventricular (LV) tissues from post-infarction chronic heart failure rats. Phosphoproteomic and proteomic analysis can provide insights regarding molecular mechanisms underlying post-infarction chronic heart failure and explore new therapeutic approaches.
2023-06-09 | PXD042843 | iProX
Project description:Three weeks after infarction, age matched rats with large infarction by ECG criteria were randomly assigned to one of the three groups: 1) Treatment with Captopril for 21 days and a daily subcutaneous dose of DITPA for the last 10 days of treatment, 2) Treatment for 10 days with DITPA alone, 3) Control heart failure and 4) Sham-operated. Keywords: Drug Effects on Heart Failure
2006-07-21 | GSE4963 | GEO
Project description:Purpose: Myocardial infarction (MI) promotes a range of systemic effects, many of which are unknown. Here, we investigated the alterations associated with MI progression in heart and other metabolically active tissues (liver, skeletal muscle, and adipose) in a mouse model of MI (induced by ligating the left ascending coronary artery) and sham-operated mice. Results: By generating tissue-specific biological networks, we observed: (1) dysregulation in multiple biological processes (including immune system, mitochondrial dysfunction, fatty-acid beta-oxidation, and RNA and protein processing) across multiple tissues post MI; and (2) tissue-specific dysregulation in biological processes in liver and heart post MI. Conclusions: Overall, our integrative analysis highlighted both common and specific biological responses to MI across a range of metabolically active tissues.
2021-04-26 | GSE153485 | GEO
Project description:Three weeks after infarction, age matched rats with large infarction by ECG criteria were randomly assigned to one of the three groups: 1) Treatment with Captopril for 21 days and a daily subcutaneous dose of DITPA for the last 10 days of treatment, 2) Treatment for 10 days with DITPA alone, 3) Control heart failure and 4) Sham-operated. Keywords: Drug Effects on Heart Failure Total RNA was prepared from left ventricle using TRIzol and later Poly A+ RNA was isolated with Oligotex beads. About 0.5ug Poly A+ RNA was reverse transcribed and labeled with Alexa Fluor 546 and 647. Labeled probed were hybridized with Operon's rat Unigene oligo library printed on glass slides. After 2 lows and 1 high stringency washes, Prolong Antifade was added to the slides to prevent any bleaching effect. The experiments were repeated 2-4 times by dye-swaping. Slides were scanned in Array Worx scanner with dual wave length. The data ratio was normalized using a location and intensity dependent Lowess formula.
2010-07-01 | E-GEOD-4963 | biostudies-arrayexpress
Project description:Myocardial infarction (MI) often results in left ventricular (LV) remodeling followed by heart failure (HF). It is of great clinical importance to understand the molecular mechanisms that trigger transition from compensated LV injury to HF and to identify relevant diagnostic biomarkers. In this study, we performed transcriptional profiling of LVs in rats with a wide range of experimentally induced infarct sizes and of peripheral blood mononuclear cells (PBMCs) in animals that developed HF. We used microarrays to investigate gene expression in the left ventricle (LV) accompanying myocardial infarction and concomitant heart failure (HF) in a well validated model of post-infarcted heart failure and to evaluate their reflection in peripheral blood mononuclear cells (PBMCs)
2013-11-15 | GSE47495 | GEO
Project description:Myocardial Infarction Model: Sixty nine animals (252 ± 2 g) were randomized to either myocardial infraction (MI) or sham operation. MI were produced by partial ligation of the left coronary artery as described in detail by Loennechen et al. (Loennechen JP, Stoylen A, Beisvag V, Wisloff U, Ellingsen O: Regional expression of endothelin-1, ANP, IGF-1, and LV wall stress in the infarcted rat heart. Am J Physiol Heart Circ Physiol 2001, 280: H2902-H2910.). Animals with large infarctions (45 ± 2% of LV) were euthanized on one of the following days: day 1 (n = 6), 3(n = 5), 7 (n = 6), 14 (n = 6), 42 (n =6) and 91 (n = 4); and sham-operated animals were euthanized on one of the following days: 1 (n = 6), 3(n = 6), 7 (n = 6), 14 (n = 6), 42 (n =6) and 91 (n = 6). After sacrifice, heart tissue was removed, weighted and scored for size of the healed infarction. Infarct size was measured and the left ventricular myocardium stored on -80°C for preparation of RNA.
2006-11-10 | E-TABM-165 | biostudies-arrayexpress
Project description:Ethnopharmacological relevance: Shexiang Baoxin Pill (SBP) is a traditional formulation of a Chinese patent medicine, which has been commonly used for the treatment of cardiovascular disease (CVD) in China since the 1980s. Previous clinical studies have shown that SBP is safe and effective in patients with CVD, but the mechanism of the therapeutic effect is still poorly understood and requires further research. Aim of the study: This study aims to comprehensively understand the effects and the underlying mechanisms of SBP for CVD treatment by analyzing the whole proteome of myocardial infarction (MI) model rats with or without SBP treatment. Materials and methods: We evaluated the therapeutic effects of SBP on myocardial infarction model (MI) rats by performing the echocardiography analyses after 15-day treatment. And the label-free quantitative proteomic approach was utilized to investigate the whole proteome of the rat heart tissues from MI group (MI rats, n=3), SBP group (MI rats treated with SBP, n=3) and SOG group (sham operated rats, n=3) on the operation day (Day 0) and 15 days after operation (Day 15), respectively. The differentially expressed proteins were subsequently analyzed with bioinformatical methods such as KEGG pathway enrichment analysis, gene ontology (GO)-annotation analysis and protein-protein interaction (PPI) network analysis. Finally, the expression levels of two promising proteins were validated by immunoblotting. Results: The echocardiography analyses show SBP significantly improved the left ventricular fractional shortening (LVFS) and left ventricular ejection fraction (LVEF) of MI rats. Additionally, 134 proteins were differentially expressed both between SBP/MI and SOG/MI, and 15 proteins were found closely related to CVD. The pathway enrichment and GO-annotation analysis of these differentially expressed proteins revealed that the proteins involved in cellular mitochondrial energy metabolism processes, such as fatty acid beta-oxidation and aerobic respiration, were significantly regulated under SBP treatments, of which fatty acid-binding protein 3 (FABP3) and myoglobin (MB) was significantly down-regulated in MI model group compared with SOG group and was returned to the basal level by SBP treatment. Expression levels of these two proteins were confirmed by immunoblotting experiments. Conclusions: These results we obtained in current study probably demonstrated that the cardio-protective effects of Shexiang Baoxin Pill might be achieved through the regulation of energy metabolism homeostasis in cardiac tissue.
2020-12-14 | PXD019296 | Pride
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.
2009-09-12 | E-GEOD-12639 | biostudies-arrayexpress
Project description:Pharmacological and gene ablation studies have demonstrated a crucial role of the caridac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. Considerable effort has been focused on the elucidation of the mechanistic underlying increased atrial ANF and BNP expression and secretion. These investigations are important because under chronic congestive heart failure, the secretion of NPs although increased and beneficial, is relatively insufficient as demonstrated by the fact that patients benefit form the unloading of the heart induced by therapeutic administration of either ANF or BNP. To identify genes involved in the transcriptional response of the endocrine heart under normal and stimulated states, we conducted differential gene expression studies of the rat atria and ventricles under normal or chronic volume overload, induced by aorto-caval shunt. The left atrial appendages and left ventricular free walls were obtained from 28 day sham and shunt operated male Sprague Dawley rats. Total RNA was obtained from three pools (of two tissues) of left atria and left ventricles under sham and shunt conditions. Three biological replicates for each muscle type and condition were generated.
2010-07-31 | E-GEOD-12754 | biostudies-arrayexpress