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.
Transcriptional profiling of left ventricle and peripheral blood mononuclear cells in a rat model of postinfarction heart failure.
Specimen part
View SamplesHeart failure (HF) is the most common cause of morbidity and mortality in the developed countries, especially considering the present demographic tendencies in those populations.
Gene expression profiling reveals potential prognostic biomarkers associated with the progression of heart failure.
Specimen part
View SamplesDespite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients.
Altered gene expression pattern in peripheral blood mononuclear cells in patients with acute myocardial infarction.
Specimen part, Subject
View SamplesWe report age-related gene expression of Treg cells isolated from injured muscle and spleen. Male C57BL/6 Foxp3-GFP reporter mice were injured intramuscularly with cardiotoxin. Tregs were sorted directly into Trizol from injured muscle and spleen 4 days post-injury. Overall design: Gene expression profiling of muscle and splenic Tregs from 2- vs >6-month old mice (biological duplicate for each).
Poor Repair of Skeletal Muscle in Aging Mice Reflects a Defect in Local, Interleukin-33-Dependent Accumulation of Regulatory T Cells.
Sex, Age, Subject
View SamplesWe report gene expression of Treg cells isolated from injured muscle in IL-33 vs PBS treated mice. Male Foxp3-GFP C57BL/6 reporter (2 months old) mice were injured intramuscularly with cardiotoxin/rIL-33 (0.3 ug/muscle). Tregs were sorted directly into Trizol from injured muscle 4 days post-injury. Overall design: Gene expression profiling of muscle Tregs from IL-33 vs PBS injured mice.
Poor Repair of Skeletal Muscle in Aging Mice Reflects a Defect in Local, Interleukin-33-Dependent Accumulation of Regulatory T Cells.
Sex, Age, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesA phenotypically and functionally distinct population of CD4+ Foxp3+ T cells (Tregs) rapidly accumulates in acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switch from a pro-inflammatory to a pro-regenerative state. Analysis of gene expression of Tregs and CD4+Foxp3- T cells (Tconvs) from injured muscle and spleen revealed that the transcriptome of muscle Treg cells is distinct from that of splenic Tregs. A set of genes is uniquely expressed by muscle Tregs, while another set is over-expressed by the two muscle populations vis--vis their two spleen counterparts.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesA comparative analysis of gene expression of injured skeletal muscle from wild-type (Foxp3-DTR-) and Treg-depleted (Foxp3-DTR+) mice showed that Treg cells are critical for effective repair and regeneration of acute injury of skeletal muscle.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment, Time
View SamplesGlobal gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs.
A special population of regulatory T cells potentiates muscle repair.
Age, Specimen part, Treatment, Time
View SamplesCD4+Foxp3+ regulatory T cells (Tregs) accumulate in skeletal muscle from dystrophin-deficient mdx mice. Analysis of global gene expression in muscles from mdx mice treated with anti-CD25 compared with muscles from mdx mice treated with control antibody revealed that Tregs partially protect mdx mice from muscle pathology and promote muscle repair/regeneration.
A special population of regulatory T cells potentiates muscle repair.
Sex, Age, Specimen part, Treatment
View Samples