The ion channel Trpc6a regulates the cardiomyocyte regenerative response to mechanical stretch
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ABSTRACT:
PROVIDER: PRJEB70944 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12352449_1.fastq.gz | Fastqsanger.gz | |||
| ERR12352449_2.fastq.gz | Fastqsanger.gz | |||
| ERR12352450_1.fastq.gz | Fastqsanger.gz | |||
| ERR12352450_2.fastq.gz | Fastqsanger.gz | |||
| ERR12352451_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Tissues and cells in organism are continuously exposed to a complicated set of mechanical cues from the environment. Mechanical stimulations affect cell proliferation, differentiation, migration, and determine tissue homeostasis as well as repair. By using a specially designed skin-stretching device, we discover hair stem cells proliferate in response to stretch and hair regeneration occurs only when proper strain and duration were delivered. Counterbalance between WNT and BMP-2 followed by a two-step mechanism was identified through molecular and genetic analyses. Macrophages were first recruited by chemokines elicited by stretch and polarized to M2 phenotype. Growth factors such as HGF and IGF-1 released by M2 macrophages then activated hair stem cells and facilitate hair regeneration. Collectively, a hierarchical control from mechanics, chemical signals, cell behaviors, to tissue responses was revealed. This novel finding shed new light on regenerative medicine and disease control since one can manipulate cellular processes through simple mechanical stimulation.
2019-01-30 | GSE125806 | GEO
Project description:With gene expression profiling it was aimed to identify the differentially expressed genes associated with the regulation of the cytoskeleton to investigate the stretch-induced cell alignment mechanism. A whole genome microarray based analysis of the stretch-induced gene expression changes was done. Gene expression was measured at the beginning of the alignment process showing first reoriented cells after 5 h stretching and at the end after 24 h, where nearly all cells are aligned. Cyclic mechanical stretching of cells results in cellular alignment perpendicular to the stretch direction regulating cellular response. This stress response is assumed to be an adaptation mechanism to reduce extensive stretching but also acts as architectural restructuring changing performance and biomechanics of the tissue. Gene expression profiling of control vs. stretched primary human dermal fibroblasts after 5 h and 24 h demonstrated the regulation of differentially expressed genes associated with metabolism, differentiation and morphology. Primary human dermal fibroblasts from ten donors were cultured on Bioflex culture plates and stretched for 5h and 24 h or left untreated to avoid changes according to cell culturing. Each of the subject provided 4 samples (control/treated and 5hrs/24hrs) resulting in 40 samples total.
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Project description:With gene expression profiling it was aimed to identify the differentially expressed genes associated with the regulation of the cytoskeleton to investigate the stretch-induced cell alignment mechanism. A whole genome microarray based analysis of the stretch-induced gene expression changes was done. Gene expression was measured at the beginning of the alignment process showing first reoriented cells after 5 h stretching and at the end after 24 h, where nearly all cells are aligned. Cyclic mechanical stretching of cells results in cellular alignment perpendicular to the stretch direction regulating cellular response. This stress response is assumed to be an adaptation mechanism to reduce extensive stretching but also acts as architectural restructuring changing performance and biomechanics of the tissue. Gene expression profiling of control vs. stretched primary human dermal fibroblasts after 5 h and 24 h demonstrated the regulation of differentially expressed genes associated with metabolism, differentiation and morphology.
2014-06-11 | GSE58389 | GEO
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Project description:The extracellular matrix (ECM) initiates mechanical cues and transduces intracellular signaling through matrix-cell interactions. The nature of cues and how they coordinate with a mechanical microenvironment are not fully understood. We identified the matricellular protein, thrombospondin-1 (Tsp1, also called Thbs1), as a mediator of matrix mechanotransduction that acts via integrin αvβ1 to establish focal adhesions and promotes nuclear shuttling of Yes-associated protein (YAP) in response to cyclic stretch. Thbs1-mediated YAP activation depends on the small GTPase Rap2 and Hippo pathway, and is not influenced by altered actin fibers. Hence, to gain insight into the molecular mechanisms underlying the Tsp1-mediated matrix mechanotransduction, we performed a comprehensive analysis of gene expression changes in Tsp1deficiant SMCs with mechanical stretch using RNA sequencing (RNA-Seq).
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Project description:Mechanical stretch induced transcriptomic profiles in cardiac myocytes II
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