Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

93 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MiRNA expression data from the hearts of murine myocardial infarction model

ABSTRACT: 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. Similar observations have been reported in murine model of MI. 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 murine MI model samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome The left anterior descending (LAD) coronary artery of mice aged 10 weeks was surgically ligated to create extensive MI. The ventricular septum of the areas at risk of ischemia was sampled on post-operative day 28. Total RNA was extracted using Sepasol solution (Sepasol-RNA I super G, nakalai tesque, Japan), and microarray analysis was performed using Affymetrix GeneChipÂ® miRNA 3.0 Arrays

ORGANISM(S): Mus musculus

SUBMITTER: Masato Tsuji

PROVIDER: E-GEOD-76592 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

miRNA expression data from human myocardial infarction hearts

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 GeneChipÂ® miRNA 3.0 Arrays

2016-01-07 | E-GEOD-76591 | biostudies-arrayexpress

miRNA expression data from human myocardial infarction hearts

2016-01-07 | GSE76591 | GEO

miRNA expression data from the hearts of murine myocardial infarction model

2016-01-07 | GSE76592 | GEO

Role of sex chromosome complement in autosomal gene expression

Project description:It has generally been assumed that most differences between males and females are due to developmental and hormonal differences between the sexes. Here we investigate the contribution of sex chromosomal complement to such sexual dimorphisms. These genome-wide transcription profiling showed that the expression of hundreds of autosomal genes was sensitive to sex chromosome complement, rather than gender. The existence of such differences between males and females holds important implications for understanding sexual dimorphisms in physiology and disease hitherto attributed solely to gender or hormonal effects. Thymic total RNA was isolated from 7-8 week old mice, with 3 biological replicates for each of four genotypes with different sex chromosome complements

2010-10-02 | E-GEOD-21822 | biostudies-arrayexpress

Kidney Transcriptome and Polycystic Kidney Disease Genes in Zebrafish

Project description:Determine if there is sexual dimorphism at the transcriptomic level in zebrafish kidneys.

2024-02-01 | GSE224859 | GEO

Transcriptome profiles of female and male mouse liver

Project description:Sexual dimorphism of gene expression is commonly observed in mammalian tissues, including liver. To assess sexual dimorphisms in gene expression, we profiled the transcriptome of liver tissue from 20-week old male and female mice of the C57BL/6N (B6) and C3H/HeN (C3) inbred mouse strains using RNA-seq. These two inbred mouse strains exhibit phenotypic differences in liver biology, as they are at opposite ends of the spectrum of spontaneous hepatocellular carcinoma incidence; C3 mice are highly susceptible to develop spontaneous liver tumors as a function of age, while B6 mice are extremely resistant. Overall, these datasets provide insight into the underlying gene expression patterns that should be considered when assessing sex differences in mouse liver.

2018-10-25 | GSE106208 | GEO

Sperm miRNA expression data from male C57BL/6J, C57BL/6J-ChrY^SJL, and C57BL/6J-ChrY^RF

Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS. miRNA expression was analyzed in epidydimal sperm pooled from 5 mice for each replicate per strain.

2015-01-16 | E-GEOD-65047 | biostudies-arrayexpress

Sexual dimorphism in osteogenic differentiation

Project description:RNA-sequencing of adult human stem cells determining sexual dimorphisms in osteogenic differentiation.

2022-03-10 | GSE185394 | GEO

Plasma miRNA Expression Profiling Using Human TaqMan Low Density Array Cards

Project description:Our study was designed to identify plasma miRNAs specific for rheumatoid arthritis (RA) by a comprehensive array approach. We performed a array-based miRNA analysis on plasma samples from three RA patients and three healthy controls (HCs). TaqMan Low-Density Array (TLDA) using human miRNA version 3.0A and version 2.0B cards (Applied Biosystems) were applied to examine the global change of miRNA expression levels in plasma from patients with RA and healthy controls. A total of 756 mature miRNA updated in the Sanger miRBase v.15.0 were quantified according to the manufacturer's instructions as previously described. Normalization was carried out with the average Ct value of all miRNAs. Relative quantification of miRNA expression was calculated with the 2−ΔΔCt Ct method. The data was presented as log10 of the relative quantity of each miRNA.

2013-04-13 | E-GEOD-46012 | biostudies-arrayexpress

Role of sex chromosome complement in autosomal gene expression

2010-10-02 | GSE21822 | GEO