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Mechanical stretch induced transcriptomic profiles in cardiac myocytes [24-48 hours]

ABSTRACT: Mechanical stretch induced transcriptomic profiles in cardiac myocytes [24-48 hours]

PROVIDER: PRJNA419924 | ENA |

REPOSITORIES: ENA

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Mechanical stretch induced transcriptomic profiles in cardiac myocytes [24-48 hours]

Project description:The effect of cyclic mecanical stretch on cardiac microRNA expression was studied in neonatal rat ventricular myocytes (NRVMs).

2018-03-17 | GSE107379 | GEO

Mechanical stretch induced transcriptomic profiles in cardiac myocytes [1-12 hours]

Project description:Mechanical stretch induced transcriptomic profiles in cardiac myocytes [1-12 hours]

| PRJNA419925 | ENA

Mechanical stretch induced transcriptomic profiles in cardiac myocytes [1-12 hours]

Project description:The effect of cyclic mecanical stretch on cardiac microRNA expression was studied in neonatal rat ventricular myocytes (NRVMs).

2018-03-17 | GSE107378 | GEO

Mechanical stretch induced transcriptomic profiles in cardiac myocytes

Project description:Mechanical stretch induced transcriptomic profiles in cardiac myocytes

| PRJNA419923 | ENA

Mechanical stretch induced transcriptomic profiles in cardiac myocytes II

Project description:Mechanical stretch induced transcriptomic profiles in cardiac myocytes II

| PRJNA420515 | ENA

Mechanical stretch induced transcriptomic profiles in cardiac myocytes II

Project description:The effect of cyclic mecanical stretch on cardiac gene expression was studied in neonatal rat ventricular myocytes (NRVMs).

2018-03-17 | GSE107551 | GEO

Manifestations of gene expression profiles in human right atrial myocardium caused by mechanical stretch

Project description:Analysis of gene expression patterns in enlarged left atrial appendage (LAA) in mitral/aortic valve replacement or coronary artery bypass graft surgery can help to identify a comprehensive panel of gene biomarkers for predicting clinical outcomes and to discover potential new therapeutic targets. However, the transcriptional profiles triggered by extended mechanical stretch in cardiac myocytes are not fully understood. Here we performed the first genome-wide study of gene expression changes in human enlarged left atium, resulting in 335 differentially expressed (> 2-fold, P < 0,05) genes in response to mechanical stretch.

2021-01-12 | GSE125094 | GEO

Comprehensive analysis of differentially expressed genes responsed to mechanical stretch in human corneal keratocytes.

Project description:Mechanical stimulation is an important factor for the development of complications after LASIK, but the molecular mechanism still remains unclear. In this study, we have employed whole genome microarray expression profiling as a discovery platform to identify genes responded to mechanical stretch in human corneal keratocytes. Furthermore, the specific signal transduction pathways were discussed. Mechanical stretch regulated gene expression was measured in human corneal keratocytes subjected to cyclic stretch (0-15% elongation, 0.5 Hz, sine waveform) for 0, 1 and 6 hours, respectively. Totally, 840 differentially expressed genes were identified in keratocytes under mechanical stretching, among which 493 genes were up-regulated and 388 genes were down-regulated. Theses differential genes were mainly involved in cytokine-cytokine receptor interaction, ECM-receptor interaction, Focal adhesion, TNF signaling pathway, and MAPK signaling pathway.

2020-12-31 | GSE124138 | GEO

Cardiac Stretch-Induced Transcriptomic Changes are Axis-Dependent

Project description:The goal of this study was to examine the effect of the major axis of biaxial mechanical stretch on cardiac myocyte gene expression and to identify the signaling pathways and transcription factors regulating these changes. Neonatal cardiac myocytes were cultured on a micropatterned substrate, and the primary stretch axis was applied either parallel or transverse to the myofibril direction. RNA sequencing was conducted to study whole genomic expression changes after acute cardiac myocyte stretch. The results showed a more robust gene response to longitudinal than to transverse stretch. After 30 minutes of stretch, 53 and 168 genes were considered differentially expressed (DE) from transverse and longitudinal stretch, respectively. After 4 hours, the number of DE genes increased to 795 in longitudinal stretch while it decreased to 35 in transverse stretch. Gene ontology term (GO) analysis indicated enrichment of TF activity and protein kinase activity by both stretch axes; whereas longitudinal but not transverse stretch caused expression of genes involved in sarcomere organization and cytoskeletal protein binding.

2019-06-01 | GSE83655 | GEO

The ion channel Trpc6a regulates the cardiomyocyte regenerative response to mechanical stretch

Project description:Myocardial damage caused for example by cardiac ischemia leads to ventricular volume overload resulting in increased stretch of the remaining myocardium. In adult mammals, these changes trigger an adaptive cardiomyocyte hypertrophic response which, if the damage is extensive, will ultimately lead to pathological hypertrophy and heart failure. Conversely, in response to extensive myocardial damage, cardiomyocytes in the adult zebrafish heart and neonatal mice proliferate and completely regenerate the damaged myocardium. We therefore hypothesized that in adult zebrafish, changes in mechanical loading due to myocardial damage may act as a trigger to induce cardiac regeneration. Based, on this notion we sought to identify mechanosensors which could be involved in detecting changes in mechanical loading and triggering regeneration. Here we show using a combination of knockout animals, RNAseq and in vitro assays that the mechanosensitive ion channel Trpc6a is required by cardiomyocytes for successful cardiac regeneration in adult zebrafish. Furthermore, using a cyclic cell stretch assay, we have determined that Trpc6a induces the expression of components of the AP1 transcription complex in response to mechanical stretch. Our data highlights how changes in mechanical forces due to myocardial damage can be detected by mechanosensors which in turn can trigger cardiac regeneration.

2023-12-20 | E-MTAB-13603 | biostudies-arrayexpress

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