Bos taurus
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ABSTRACT:
PROVIDER: PRJNA94781 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We tested the hypothesis that cholinergic stimulation (via treatment with carbachol) and cyclic stretch regulate inflammatory gene expression in intact airway smooth muscle by measuring mRNA expression in bovine tracheal smooth muscle. Keywords: response to stress and drug
2006-02-23 | GSE4287 | GEO
Project description:The aim of the experiment was to determine the effect of cyclic stretch-relaxation ("stretch") on gene expression patterns in normal diploid human bladder smooth muscle cells. Cells plated on silicone elastomer bottomed 6-well culture dishes were grown to ~80% confluence, serum-depleted for 48h and subjected to cyclic stretch-relaxation at 20% elongation for 4h. Cells seeded in stretch plates but not subjected to stretch served as controls. Total RNA was extracted from both groups of cells, reverse-transcribed, biotin-labeled, fragmented and hybridized to HG-U133A. Four biological replicates were generated for each treatment group (non-stretched or stretched). Keywords = bladder Keywords = smooth muscle cells Keywords = cyclic stretch-relaxation Keywords: other
2004-11-04 | GSE1595 | GEO
Project description:The aim of the experiment was to determine the effect of cyclic stretch-relaxation ("stretch") on gene expression patterns in normal diploid human bladder smooth muscle cells. Cells plated on silicone elastomer bottomed 6-well culture dishes were grown to ~80% confluence, serum-depleted for 48h and subjected to cyclic stretch-relaxation at 20% elongation for 4h. Cells seeded in stretch plates but not subjected to stretch served as controls. Total RNA was extracted from both groups of cells, reverse-transcribed, biotin-labeled, fragmented and hybridized to HG-U133A. Four biological replicates were generated for each treatment group (non-stretched or stretched).
2007-08-04 | E-GEOD-1595 | biostudies-arrayexpress
Project description:PGC1α regulates the mitochondrial metabolism response to cyclic stretch, which inhibits neointimal hyperplasia microscopy revealed that intimal injury disrupted the balance of vascular energy metabolism and impaired the mitochondrial ultrastructure in vivo. The human carotid plaque and femoral artery plaque samples also exhibited alterations in mitochondrial morphology. Vascular smooth muscle cells (VSMCs) are the main components of neointimal hyperplasia and are subjected to cyclic stretch resulting from pulsatile pressure. In this study, we found that the application of cyclic stretch in vitro increased VSMC mitochondrial mass and function. In addition, peroxisome proliferator-activated receptor gamma coactivator-1α (PGC1α) played an important role in regulating VSMC mitochondrial function in response to physiological stretch via the phosphorylation of Smad3. Increasing the activation of PGC1α by ZLN005 treatment effectively inhibited VSMC hyperproliferation after intimal injury in vivo. These results suggested that the regulation of PGC1α by p-Smad3 in response to physiological cyclic stretch may effectively alleviate neointimal hyperplasia by promoting mitochondrial function. PGC1α may be a potential therapeutic target for the prevention and treatment of neointimal hyperplasia.
2025-08-13 | GSE285663 | GEO
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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).
2009-08-31 | GSE16650 | GEO
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