Effect of mechanically responsive miRNAs on biomechanical properties of airway smooth muscle cells and their related drug development studies
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PROVIDER: PRJNA850789 | ENA |
REPOSITORIES: ENA
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Project description:In the short two decades since microRNAs (miRNAs) were discovered, scientists have focused more attention on the biological field of miRNAs. A deeper understanding of the role of miRNAs in development and disease has made miRNAs a powerful tool and target for new therapeutic approaches. However, whether miRNAs are involved in the response of ASMCs to high stretch and high matrix stiffness and their underlying mechanisms remain unclear, especially the relationship between the expression of miRNAs and the biomechanical behavior of ASMCs remains unclear. In this study, we combined bioinformatics and cell mechanics approaches to screen stretch-sensitive and matrix stiffness-sensitive miRNAs and investigate their effects on the biomechanical behaviors of ASMCs.
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Project description:Vascular smooth muscle cells (VSMCs) respond to biomechanical stretch with specific changes in gene expression which govern the phenotype of these cells. The mechanotransducer zyxin is a potential candidate for regulating the expression of such genes. Using microarrays, we compared stretch-induced gene expression in wild type and zyxin-null VSMCs to define such changes in detail.
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Project description:Selective stimulation of IL-4 receptor on smooth muscle induces airway hyper-responsiveness in mice. Abstract: Production of the cytokines IL-4 and IL-13 is increased in both human asthma and mouse asthma models and Stat6 activation by the common IL-4/IL-13R drives most mouse model pathophysiology, including airway hyperresponsiveness (AHR). However, the precise cellular mechanisms through which IL-4Rα induces AHR remain unclear. Overzealous bronchial smooth muscle constriction is thought to underlie AHR in human asthma, but the smooth muscle contribution to AHR has never been directly assessed. Furthermore, differences in mouse vs. human airway anatomy and observations that selective IL-13 stimulation of Stat6 in airway epithelium induces murine AHR raise questions about the importance of direct IL-4R effects on smooth muscle in murine asthma models and relevance of these models to human asthma. Using transgenic mice in which smooth muscle is the only cell type that expresses or fails to express IL-4Rα, we demonstrate that direct smooth muscle activation by IL-4, IL-13, or allergen is sufficient, but not necessary, to induce AHR and show that 5 genes known to promote smooth muscle migration, proliferation and contractility are activated by IL-13 in smooth muscle in vivo. These observations demonstrate that IL-4Rα promotes AHR through multiple mechanisms and provide a model for testing smooth muscle-directed asthma therapeutics.
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