Mus musculus
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ABSTRACT:
PROVIDER: PRJNA100305 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression microarray profiling in mice hearts with pathological and physiological cardiac hypertrophy
| PRJNA242995 | ENA
Project description:miRNA-99 family diverges physiological cardiac hypertrophy to pathological cardiac hypertrophy
| PRJNA297403 | ENA
Project description:Loss of mouse P2Y6 nucleotide receptor is associated with physiological macrocardia and amplified pathological cardiac hypertrophy
| PRJNA306654 | ENA
Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure. Small RNA profiles of control and hypertrophied cardiomyocyte H9c2 cells were generated by deep sequencing using Illumina HiSeq 2000
2015-11-01 | E-GEOD-73597 | biostudies-arrayexpress
Project description:Purpose: The physiological cardiac hypertrophy is an adaptive condition that does not associate with myocyte cell death while pathological hypertrophy is a maladaptive condition associated with myocyte cell death. Alpha-2 macroglobulin (α-2M) an acute phase protein induces cardiac hypertrophy via the ERK1,2 and PI3K/Akt signaling. This study is aimed at exploring the miRNome of α-2M induced hypertrophied cardiomyocytes and to understand the role of miRNAs in determination of pathological and physiological hypertrophy. Methods: Hypertrophy was induced in H9c2 cardiomyoblasts using alpha-2 macroglobulin. The induction of hypertrophy is confirmed by microscopy and gene expression studies. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during hypertrophy. Among the differentially expressed candidates, miR-99 family (miR-99a, miR-99b and miR-100) showed significant downregulation upon α-2M treatment while isoproterenol treatment (pathological hypertrophy) upregulated their expression. The binding site for Egr1 transcription factor was identified in the promoter region of miR-99 family, and interestingly all miRNAs with Egr1 binding site proven by ChIP-Seq were downregulated during physiological hypertrophy Conclusions: The results proved Egr-1 mediated regulation of miR-99 family determines the uniqueness of pathological and physiological hypertrophy. Upregulated miR-99 expression during pathological hypertrophy suggests that it can be a valuable diagnostic marker and potential therapeutic target for cardiac hypertrophy and heart failure.
2015-11-01 | GSE73597 | GEO
Project description:We performed microarray analyses on RNA from mice with isoproterenol-induced cardiac hypertrophy and mice with exercise-induced physiological hypertrophy and identified 865 and 2,534 genes that were significantly altered in pathological and physiological cardiac hypertrophy models, respectively.
2009-10-31 | GSE18801 | GEO
Project description:Purpose: Different studies revealed the importance of microRNAs (miRNAs) in pathological hypertrophy but their role during physiological hypertrophy is largely unexplored. Hence, this study is aimed at revealing the global expression profile of miRNAs during physiological cardiac hypertrophy. Methods: Chronic swimming protocol continuously for eight weeks resulted in induction of physiological hypertrophy in rats and histopathology revealed the absence of tissue damage, apoptosis or fibrosis. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during physiological hypertrophy. The expression profile of the significantly differentially expressed miRNAs were validated by qPCR. Conclusions: This is the first report to reveal the involvement of a large number of apoptotic miRNAs during physiological cardiac hypertrophy including the previously unknown cardiac players like miR-99, miR-100, miR-191, miR-181 and miR-19. Our data indicates that regulation of these apoptotic miRNAs can be one of the major key factor in determining pathological or physiological hypertrophy by controlling apoptosis, fibrosis and cell death mechanisms.
2015-10-31 | GSE62883 | GEO
Project description:Cardiac hypertrophy can lead to heart failure, and is induced either by physiological stimuli eg postnatal development, chronic exercise training or pathological stimuli eg pressure or volume overload. Majority of new therapies for heart failure has mixed outcomes. A combined mouse model and oligo-array approach are used to examine whether phosphoinositide 3-kinase (p110-alpha isoform) activity is critical for maintenance of cardiac function and long-term survival in a setting of heart failure. The significance and expected outcome are to recognise genes involved in models of heart failure ie pathological- vs physiology-hypertrophy, and examine the molecular mechanisms responsible for such activity. Growth of the heart can be induced by physiological stimuli e.g., postnatal development, chronic exercise training, or pathological stimuli e.g., pressure or volume overload. Physiological hypertrophy (“good”) is characterised by a normal organisation of cardiac structure, and normal or enhanced cardiac function. In comparison, pathological hypertrophy (”bad”) is associated with fibrosis, cardiac dysfunction, and increased morbidity and mortality. The mechanistic process which allows the heart to enlarge in response to physiological stimuli while maintaining normal or enhanced function is of great clinical relevance because one potential therapeutic strategy is to inhibit the pathological growth process while augmenting the physiological growth process. One of the major process that regulate heart size is by phosphoinositide 3-kinase (PI3K). Thus the end goal of this project is to determine whether the p110 alpha isoform of PI3K could be a potential tool for augmenting physiological growth and improving cardiac function of the failing diseased heart, and to examine the underlying mechanisms responsible. Keywords: Disease progression analysis
2010-03-08 | GSE7487 | GEO
Project description:Purpose: Different studies revealed the importance of microRNAs (miRNAs) in pathological hypertrophy but their role during physiological hypertrophy is largely unexplored. Hence, this study is aimed at revealing the global expression profile of miRNAs during physiological cardiac hypertrophy. Methods: Chronic swimming protocol continuously for eight weeks resulted in induction of physiological hypertrophy in rats and histopathology revealed the absence of tissue damage, apoptosis or fibrosis. Subsequently, the total RNA was isolated and small RNA sequencing was executed in Illumina HiSeq 2000. Results: Analysis of small RNA reads revealed the differential expression of a large set of miRNAs during physiological hypertrophy. The expression profile of the significantly differentially expressed miRNAs were validated by qPCR. Conclusions: This is the first report to reveal the involvement of a large number of apoptotic miRNAs during physiological cardiac hypertrophy including the previously unknown cardiac players like miR-99, miR-100, miR-191, miR-181 and miR-19. Our data indicates that regulation of these apoptotic miRNAs can be one of the major key factor in determining pathological or physiological hypertrophy by controlling apoptosis, fibrosis and cell death mechanisms. Heart small RNA profiles of 16-week old control and physiologically hypertrophied wistar rat were generated by deep sequencing using Illumina HiSeq 2000
2015-10-31 | E-GEOD-62883 | biostudies-arrayexpress
Project description:The heart grows in response to pathological and physiological stimuli, while the former often precedes cardiomyocyte loss and heart failure, the latter paradoxically protects the heart and enhances cardiomyogenesis. Long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. The purpose of this study was to compare transcriptome profilings in exercise-induced physiological cardiac growth and stress-induced pathological cardiac growth. We identified a set of lncRNAs called long noncoding exercise associated cardiac transcripts (lncExACT). One of them, lncExACT1, whose cardiac expression was downregulated after exercise but upregulated after transverse aortic constriction. Inhibition of lncExACT1 induced physiolgoical cardiac growth while overexpression of lncExACT1 induced pathological hypertrophy and heart failure.
2022-10-18 | GSE186081 | GEO