Expression data from cultured rat right ventricular papillary muscles
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE45250 | GEO | 2013/03/19
SECONDARY ACCESSION(S): PRJNA193317
REPOSITORIES: GEO
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Project description:Several different mechanical signals have been proposed to control the extent and pattern of myocardial growth and remodeling, though this has largely been studied using in vitro model systems that are not representative of intact myocardium or in vivo models in which isolating the effects of individual candidate stimuli is exceedigly difficult. We used a unique tissue culture system that allows the simultaneous control of multiple mechanical inputs and other potentially confounding stimuli (e.g., hormonal). Following a 12 hour culture period under prescribed mechanics, we used microarrays to identify genes that are up- or down-regulated in response to different amounts of mean stretch and cyclic shortening. Muscles were dissected (one from each of 12 different male LBN-F1 rats) and cultured for 12 hours in a pseudo-sterile muscle culture system under one of four mechanical input schemes (i.e., three biological replicates per mechanical input group). We prescribed low or high values of both time averaged stretch and cyclic shortening. Specifically, we targeted 4% or 16% mean stretch (from slack length) and 4% of 16% cylic shortening (% of slack length) over the 12 hour culture period to give the following four groups: high mean stretch x high shortening (group A); high mean stretch x low shortening (group B); low mean stretch x low shortening (group C); low mean stretch x high shortening (group D). This 2 x 2 factorial design allowed us to identify individual genes and/or molecular pathways that might be regulated by one or both of these mechanical inputs indpendent from other candidate mechanical or hormonal stimuli.
2013-03-19 | E-GEOD-45250 | biostudies-arrayexpress
Project description:AVICs were exposed to cyclic stretch to examine the role of mechanical stimuli on gene expression AVICs cultured on collagen 1 coated Bioflex were exposed to 14% stretch at 1 hz or static conditions using a Flexcell-5000 14% stretch was the experimental condition while the static condition was the control
2015-01-09 | E-GEOD-47687 | biostudies-arrayexpress
Project description:AVICs were exposed to cyclic stretch to examine the role of mechanical stimuli on gene expression AVICs cultured on collagen 1 coated Bioflex were exposed to 14% stretch at 1 hz or static conditions using a Flexcell-5000
2015-01-09 | GSE47687 | GEO
Project description:Engineered cardiac tissues (ECTs) are platforms to investigate cardiomyocyte maturation and functional integration, to evaluate the feasibility of generating implantable tissues for cardiac repair and regeneration, and may be useful models for pharmacology and toxicology bioassays. These ECTs rapidly mature in vitro to acquire the features of functional cardiac muscle and respond to mechanical load with increased proliferation and maturation. ECTs can be generated from various immature cardiac cell sources and little is known regarding the broad changes in regulatory transcript expression that occur in these in vitro tissues during normal maturation and in response to mechanical or pharmacologic interventions. We tested the hypothesis that global ECT gene expression patterns are sensitive to mechanical loading conditions and tyrosine kinase inhibitors, similar to the maturing myocardium. We generated 3D ECTs from day 14.5 rat embryo ventricular cells, as previously published, and then treated constructs after 5 days in culture for 48 hours with mechanical stretch (5%, 0.5 Hz) and/or the p38MAPK (p38 mitogen-activated protein kinase) selective inhibitor BIRB796. RNA was isolated from 3 sets of experiments and assayed using a standard Agilent rat 4x44k V3 microarray and Pathway Analysis software for transcript expression fold changes and changes in regulatory molecules and networks. At the threshold of a 1.5 fold change in expression, mechanical stretch altered 1,559 transcripts, versus 1,411 for BIRB796, and 1,846 for stretch plus BIRB796. As anticipated, top pathways altered in response to these stimuli include Cellular Development, Cellular Growth and Proliferation; Tissue Development; Cell Death, Cell Signaling, and Small Molecule Biochemistry as well as numerous other pathways. Changes in transcript expression were confirmed by quantitative-PCR for selected regulatory molecules. Thus, ECTs display a broad spectrum of altered gene expression in response to mechanical load and/or tyrosine kinase inhibition, reflecting the complex regulation of proliferation, differentiation, and architectural alignment that occurs during ECT maturation and adaptation. This approach can now be used to test the role of individual molecules and pathways on the regulation of ECT maturation and remodeling. 7 and 4 biological replicates with four groups (control, mechanical stretch, BIRB and mechanical stretch with BIRB)
2016-06-25 | E-GEOD-48342 | biostudies-arrayexpress
Project description:Acute respiratory distress syndrome (ARDS) is a catastrophic form of acute lung injury (ALI). The necessity for mechanical ventilation (MV) renders patients at risk for ventilator induced lung injury (VILI). Exposure to repetitive cyclic stretch (CS) and/or over-inflation exacerbates injury. Reducing tidal volume (VT) is the only therapeutic strategy shown to mitigate morbidity and mortality. Cyclic stretch has been shown to differentially regulate gene expression in part through the activation of mammalian mitogen-activated protein kinase (MAPK). Although these studies have shown both molecular and cellular alterations, no unifying hypothesis to explain MV-induced lung injury has emerged. In the current study, we hypothesized that coordinated expression of cyclic stretch (CS)-responsive genes relies on the presence of common CS-sensitive regulatory elements. To identify CS-responsive genes, we undertook a comparative examination of the gene expression profile of human bronchial epithelial airway (Beas-2B) cells in response to various injurious stimuli involved in the pathogenesis of acute lung injury (ALI)/Ventilator induced lung injury (VILI): cyclic stretch, tumor necrosis factor alpha (TNF-a), and lipopolysaccharide (LPS). Experiment Overall Design: Human Bronchial Epithelial Cells (Beas-B2) cells grown on silicon elastic plates coated with Type I collagen (Flexercell International, McKeesport, PA) were exposed to six regiments for 4 h: 1) control (static, [control]); 2) mechanical stretch (25 PKa, 30 cycles per min, [stretch]); 3) LPS (1 mcg/ml [LPS]); 4) TNF-α (20 ng/ml; [TNF]); 5) mechanical stretch plus LPS [LPS+S], and 6) mechanical stretch plus TNF-α [TNF+S]. Total RNA (duplicate experiments) was extracted using TRIZOL reagent (as per manufactures specifications) and purified using Qiagen mRNA purification Kit (as per manufacturers specifications). mRNA was hybridized to Affymetrix Human U133plus2.0 chips. Probe based analysis, background reduction, and quantile data normalization was performed in MeV 4.0 of TM4 using Robust Multi-array Average (RMA).
2009-09-15 | E-GEOD-16650 | biostudies-arrayexpress
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:ObjectiveArrhythmogenic mitral valve prolapse (MVP) is an important cause of sudden cardiac death characterized by fibrosis of the papillary muscles or left ventricle (LV) wall, and an association between late gadolinium enhancement (LGE) of the LV papillary muscles and ventricular arrhythmia in MVP has been reported. However, LGE of the papillary muscles may be observed in other causes of mitral regurgitation, and it is not limited to patients with MVP. This study was to evaluate the association of LGE of the LV papillary muscles or ventricular wall on cardiac magnetic resonance imaging (CMR) and ventricular arrhythmia in patients with mitral regurgitation.Materials and methodsThis study included 88 patients (mean age ± standard deviation, 58.3 ± 12.0 years; male, 42%) with mitral regurgitation who underwent CMR. They were allocated to the MVP (n = 43) and non-MVP (n = 45) groups, and their LGE images on CMR, clinical characteristics, echocardiographic findings, and presence of arrhythmia were compared.ResultsLV myocardial wall enhancement was more frequent in the MVP group than in the non-MVP group (28% vs. 11%, p = 0.046). Papillary muscle enhancement was observed in 7 (7.9%) patients. Of the 43 patients with MVP, 15 (34.8%) showed LGE in the papillary muscles or LV myocardium, including 12 (27.9%) with LV myocardial wall enhancement and 4 (9.3%) with papillary muscle enhancement. One patient with bilateral diffuse papillary muscle enhancement experienced sudden cardiac arrest due to ventricular fibrillation. Univariable logistic regression analysis showed that high systolic blood pressure (BP; odds ratio [OR], 1.05; 95% confidence interval [CI], 1.01-1.09; p = 0.027) and ventricular arrhythmia (OR, 6.84; 95% CI, 1.29-36.19; p = 0.024) were significantly associated with LGE of the papillary muscles.ConclusionLGE of the papillary muscles was present not only in patients with MVP, but also in patients with other etiologies of mitral regurgitation, and it was associated with high systolic BP and ventricular arrhythmia. Papillary muscle enhancement on CMR should not be overlooked.
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Project description:Engineered cardiac tissues (ECTs) are platforms to investigate cardiomyocyte maturation and functional integration, to evaluate the feasibility of generating implantable tissues for cardiac repair and regeneration, and may be useful models for pharmacology and toxicology bioassays. These ECTs rapidly mature in vitro to acquire the features of functional cardiac muscle and respond to mechanical load with increased proliferation and maturation. ECTs can be generated from various immature cardiac cell sources and little is known regarding the broad changes in regulatory transcript expression that occur in these in vitro tissues during normal maturation and in response to mechanical or pharmacologic interventions. We tested the hypothesis that global ECT gene expression patterns are sensitive to mechanical loading conditions and tyrosine kinase inhibitors, similar to the maturing myocardium. We generated 3D ECTs from day 14.5 rat embryo ventricular cells, as previously published, and then treated constructs after 5 days in culture for 48 hours with mechanical stretch (5%, 0.5 Hz) and/or the p38MAPK (p38 mitogen-activated protein kinase) selective inhibitor BIRB796. RNA was isolated from 3 sets of experiments and assayed using a standard Agilent rat 4x44k V3 microarray and Pathway Analysis software for transcript expression fold changes and changes in regulatory molecules and networks. At the threshold of a 1.5 fold change in expression, mechanical stretch altered 1,559 transcripts, versus 1,411 for BIRB796, and 1,846 for stretch plus BIRB796. As anticipated, top pathways altered in response to these stimuli include Cellular Development, Cellular Growth and Proliferation; Tissue Development; Cell Death, Cell Signaling, and Small Molecule Biochemistry as well as numerous other pathways. Changes in transcript expression were confirmed by quantitative-PCR for selected regulatory molecules. Thus, ECTs display a broad spectrum of altered gene expression in response to mechanical load and/or tyrosine kinase inhibition, reflecting the complex regulation of proliferation, differentiation, and architectural alignment that occurs during ECT maturation and adaptation. This approach can now be used to test the role of individual molecules and pathways on the regulation of ECT maturation and remodeling.
2016-06-25 | GSE48342 | GEO
Project description:Alveolar epithelial type II (AEII) cells are the first line host in response to mechanical ventilation. We tested the hypothesis that the modulation of microRNA on AEII cells in response to mechanical stretch may participate in the ventilator-induced lung injury. This experiment is designed to screen miRNAs that are deregulated during mechanical stretch of AEII cells.
2015-11-18 | GSE75100 | GEO
Project description:Formation of oriented myofibrils is a key event in the development of a functional musculoskeletal system. However, the mechanisms that control orientation of myocytes, their fusion and the resulting directionality of adult muscles remain enigmatic. Here, we utilized in vivo and in vitro live imaging, CAS9/CRISPR-mediated mutagenesis in fish, genetic experiments in mice and single cell transcriptomics to demonstrate that individual myocyte polarization and subsequent orientation depend on cell stretch imposed by skeletal expansion. Our data revealed that upon migration, individual facial myocytes form unpolarized clusters corresponding to future muscle groups. These clusters undergo oriented stretch and alignment during embryonic growth. Experimental in vivo perturbations of cartilage shape, size and distribution caused disruptions in directionality and number of myofibrils. Controlled in vitro 2D and 3D experiments applying continuous tension via artificial attachment points demonstrated a sufficiency for mechanical forces to instruct coherent polarization of myocyte populations. Consistently, perturbations of cartilage extension revealed a role of the developing skeleton in the directional outgrowth of non-muscle soft tissues during limb and facial morphogenesis.
2020-10-27 | GSE160098 | GEO