Gene expression patterns from mice hearts with myocardial infarction pretreated with miR-433 inhibition or not
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE74206 | GEO | 2017/02/12
SECONDARY ACCESSION(S): PRJNA299319
REPOSITORIES: GEO
Similar Datasets
Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome Human tissue samples, acquired during post-mortem examination and frozen in liquid nitrogen, were provided by the department of pathology, Tokyo Metropolitan Geriatric Hospital after the approval from the ethical committee. Age- and sex-matched cohorts were selected to compare healthy hearts to those with post-MI LV remodeling. Border zone for myocardial infarction was sampled. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChip® miRNA 3.0 Arrays
2016-01-07 | E-GEOD-76591 | biostudies-arrayexpress
Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.
2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress
Project description:Myocardial regeneration capacity declines during the first week after birth and is linked to the adaptation to oxidative metabolism. Utilizing this regenerative window, we characterized the transcriptomic changes in myocardial injury in 1-day-old regeneration-competent and 7-day-old regeneration-compromised mice. The mice were either sham-operated or received left anterior descending coronary artery ligation to induce myocardial infarction and acute ischemic heart failure. Myocardial tissue samples were collected after 3- and 21-day follow-up period. Whole transcriptome and miRNA NGS data was analyzed. We identified specific time-dependent transcription factors and networks contributing to both regeneration competence and failure.
2022-12-31 | GSE198301 | GEO
Project description:Myocardial regeneration capacity declines during the first week after birth and is linked to the adaptation to oxidative metabolism. Utilizing this regenerative window, we characterized the transcriptomic changes in myocardial injury in 1-day-old regeneration-competent and 7-day-old regeneration-compromised mice. The mice were either sham-operated or received left anterior descending coronary artery ligation to induce myocardial infarction and acute ischemic heart failure. Myocardial tissue samples were collected after 3- and 21-day follow-up period. Whole transcriptome and miRNA NGS data was analyzed. We identified specific time-dependent transcription factors and networks contributing to both regeneration competence and failure.
2022-12-31 | GSE198300 | GEO
Project description:Mice with homozygous null mutations in the HDL receptor (SR-BI) and apoE genes (SR-BI KO/apoE double KO (dKO) mice) spontaneously develop occlusive, atherosclerotic coronary artery disease (CAD) and die prematurely (50% mortality at 42 days of age) on standard chow diet feeding. Microarray analysis was performed to investigate the changes in gene expression profiles during the development of spontaneous severe CAD, which includes myocardial infarction and heart failure. These data will provide new insights in understanding the pathophysiology of CAD. The whole Hearts from dKO or SR-BI+/- apoE-/- (HET) mice (n=9-12) were harvested at 21, 31 and 43 days of age, and analyzed using Affymetrix microarrays. dKO mice do not show detectable signs of CAD at 21 days of age, small myocardial infarction (MI) and heart failure at 31 days of age, and extensive MI and severe heart failure at 43 days of age (50% mortality at 42 days of age). Each mouse was assigned to one array. SR-BI+/- apoE-/- mice (HET) which do not develop detectable signs of CAD on chow diet were used as controls.The data also include those from probucol treated dKO and HET mice (n=2-8).
2013-09-01 | E-GEOD-49937 | biostudies-arrayexpress
Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of human MI samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome
2016-01-07 | GSE76591 | GEO
Project description:The Myocardial Infarction Platelet Transcriptome
| PRJNA1135265 | ENA
Project description:Despite 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. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.
2014-10-23 | E-GEOD-62646 | biostudies-arrayexpress
Project description:Survivors of myocardial infarction are at increased risk for vascular dementia. Neuroinflammation has been implicated in the pathogenesis of vascular dementia, yet little is known about the cellular and molecular mediators of neuroinflammation after myocardial infarction. Using a mouse model of myocardial infarction coupled with flow cytometric analyses and immunohistochemistry, we discovered increased monocyte abundance in the brain after myocardial infarction, which was associated with increases in brain-resident perivascular macrophages and microglia. Myeloid cell recruitment and activation was also observed in post-mortem brains of humans that died after myocardial infarction. Spatial and single cell transcriptomic profiling of brain-resident myeloid cells after experimental myocardial infarction revealed increased expression of monocyte chemoattractant proteins. In parallel, myocardial infarction increased crosstalk between brain-resident myeloid cells and oligodendrocytes, leading to neuroinflammation, white matter injury, and cognitive dysfunction. Inhibition of monocyte recruitment preserved white matter integrity and cognitive function, linking monocytes to neurodegeneration after myocardial infarction. Together, these preclinical and clinical results demonstrate that monocyte infiltration into the brain after myocardial infarction initiate neuropathological events that lead to vascular dementia.
2025-05-21 | GSE268156 | GEO
Project description:microRNAs control cardiac remodeling post myocardial infarction, though the cellular and molecular mechanisms remain unclear. We used microarrays to examine microRNA profiles in mice hearts 21 days after ligation of left anterior descending coronary artery (LAD) versus sham control.
2017-02-12 | GSE74135 | GEO