Analysis of transcriptional changes in heart after deletion of AK079912
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER:
PROVIDER: E-MTAB-13048 | biostudies-arrayexpress |
SECONDARY ACCESSION(S): E-MTAB-13047
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Ischemia reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation, leading to graft failures and lower long-term survival rate of the recipient. IR causes apoptosis / death of cardiomyocytes, resulting from up-regulation of apoptotic genes and down-regulation of anti-apoptotic genes. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. We used microarrays to detect gene expression profile of ischemia reperfusion injured hearts and identified distinct classes of up-regulated and down regulated genes during this I/R.
2013-09-17 | E-GEOD-50884 | biostudies-arrayexpress
Project description:Interferon regulatory factor 2 binding protein 2 (Irf2bp2), a co-repressor of Irf2, is required for fetal hepatic erythropoiesis through the expansion of erythromyeloid progenitors. Mice with germline ablation of the entire Irf2bp2 transcript produced no viable Irf2bp2-null (knockout, KO) pups in first litters. In subsequent litters, fewer than 1/3 of the expected KO pups were born and half survived to adulthood. Heart, skeletal muscle and liver tissues (tissues with high Irf2bp2 expression) were acquired from WT and KO mice, followed by RNA extraction using the RNeasy Midi Kit and subsequent gene expression profiling using the Affymetrix Mouse Gene 1.0 ST v1 array. Transcriptome profiles of surviving KO mice were contrasted to WT mice giving insight to modified gene expression in the absence of Irf2bp2 across multiple vital tissues.
2023-02-02 | E-MTAB-11558 | biostudies-arrayexpress
Project description:We deleted Tfr1 in the heart to determine the role of Tfr1 in iron uptake in normal cardiac funciton We used microarrays to identify global gene changes associated with deletion of Tfr1 in skeletal muscle We isolated RNA from WT and Tfr1 KO hearts at both postnatal day 5 and postnatal day 10.RNA was labaled and hibridized to Affymetrics microarrays.
2015-05-12 | E-GEOD-68745 | biostudies-arrayexpress
Project description:The zebrafish has the capacity to regenerate its heart after severe injury. While the function of a few genes during this process has been studied, we are far from fully understanding how genes interact to coordinate heart regeneration. To enable systematic insights into this phenomenon, we generated and integrated a dynamic co-expression network of heart regeneration in the zebrafish and linked systems-level properties to the underlying molecular events. Across multiple post-injury time points, the network displays topological attributes of biological relevance. We show that regeneration steps are mediated by modules of transcriptionally coordinated genes, and by genes acting as network hubs. We also established direct associations between hubs and validated drivers of heart regeneration with murine and human orthologs. The resulting models and interactive analysis tools are available at http://infused.vital-it.ch. Using a worked example, we demonstrate the usefulness of this unique open resource for hypothesis generation and in silico screening for genes involved in heart regeneration. In order to monitor the whole regeneration process, we recovered samples at different time points post-injury: 4 h, 1 day, 3 days, 7 days, 14 days and 90 days (respectively 4 hpi, 1 dpi, 3 dpi, 7 dpi, 14 dpi and 90 dpi). Cryoinjured hearts were compared to healthy hearts from control fish in 3 independent experiments.
2016-06-01 | E-GEOD-67665 | biostudies-arrayexpress
Project description:Mice with germline deletion of AK079912 were used to analyze transcriptional changes in brown adipose tissue.
2024-03-27 | E-MTAB-13047 | biostudies-arrayexpress
Project description:Genome-wide association studies have identified a small region at chromosome 9p21.3 strongly associated with coronary heart disease risk. The region contains no protein-coding genes and the mechanism underlying its association with heart disease is unknown. We investigated associations between rs1333049, a single nucleotide polymorphism representing the 9p21.3 locus, and levels of cardiac gene expression in myocardial tissue from donors with no documented history of heart disease. Individual myocardial gene expression profiles were generated with Affymetrix Human Gene 1.0 ST arrays (n=108). DNA genotyping was performed with Taqman assays. Associations between genotype and gene expression were analyzed assuming a recessive effect.
2012-07-03 | E-GEOD-22253 | biostudies-arrayexpress
Project description:Analysis of alternative splicing of left ventricles heart samples of 3 DM1 adult versus 3 adult controls PolyA RNA from left ventricles (heart) of 3 controls and 3 DM1 patients were analysed on Exon Array (Affymetrix)
2016-01-21 | E-GEOD-67067 | biostudies-arrayexpress
Project description:Ischemia reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation, leading to graft failures and lower long-term survival rate of the recipient. microRNAs are major regulators of genes. IR causes apoptosis/death of cardiomyocytes, resulting from up-regulation of apoptotic genes and down-regulation of anti-apoptotic genes which are regulated by microRNA. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. We perserved donor hearts with university of Wisconsin solution for 18h at 4C degree before being implanted into recipients to create ischemia reperfusion injury. The preserved hearts were implanted into a syngeneic recipient mice. 24h after transplantation, heart grafts were harvested for microRNA extraction.
2013-09-17 | E-GEOD-50885 | biostudies-arrayexpress
Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.
2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress
Project description:This study was conducted to examine normal gene expression in the heart during mouse embryonic development. Wild type embryo hearts (n=5) were collected at stage E12.5 and total RNA was isolated for analysis by Affymetrix mouse genome 430A GeneChip.
2010-07-08 | E-GEOD-17935 | biostudies-arrayexpress