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Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program [ATAC-seq]

ABSTRACT: Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program [ATAC-seq]

PROVIDER: PRJNA998539 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25422200_1.fastq.gz	Fastqsanger.gz
	SRR25422200_2.fastq.gz	Fastqsanger.gz
	SRR25422201_1.fastq.gz	Fastqsanger.gz
	SRR25422201_2.fastq.gz	Fastqsanger.gz
	SRR25422202_1.fastq.gz	Fastqsanger.gz

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Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program

Project description:Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program

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Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program [RNA-seq]

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Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program [ATAC-seq]

Project description:Tissue resident macrophages play important roles in tissue homeostasis and repair. However, how macrophages monitor and maintain tissue integrity is not well understood. The extracellular matrix (ECM) is a key structural and organizational component of all tissues. Here, we find that macrophages sense the mechanical properties of the ECM in order to regulate a specific tissue repair program. We show that macrophage mechanosensing is mediated by cytoskeletal remodeling and can be performed in three-dimensional environments through a non-canonical, integrin-independent mechanism analogous to amoeboid migration. We find that these cytoskeletal dynamics also integrate biochemical signaling by CSF1 and ultimately regulate chromatin accessibility to control the mechanosensitive gene expression program. This study suggests a distinct mode of ECM mechanosensing and growth factor signaling through which macrophages may regulate tissue repair and fibrosis.

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Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program [RNA-seq]

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Macrophages sense ECM mechanics and growth factor availability through cytoskeletal remodeling to regulate their tissue repair program

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YAP regulates cell mechanics by controlling focal adhesion assembly

Project description:Hippo effectors YAP/TAZ act as on-off mechanosensing switches by sensing modifications in extracellular matrix (ECM) composition and mechanics. The regulation of their activity has been described so far through a hierarchical model in which elements of Hippo pathway are under the control of Focal Adhesions (FAs). Here we unveiled the molecular mechanism by which cell spreading and RhoA GTPase control FA formation through YAP to stabilize the anchorage of actin cytoskeleton to cell membrane. This mechanism required YAP co-transcriptional function and involved the activation of genes encoding for integrins and FA docking proteins. Tuning YAP transcriptional activity led to the modification of cell mechanics, force development, adhesion strength, determined cell shaping, migration and differentiation. These results provide new insights into the mechanism of YAP mechanosensing activity and qualify Hippo effector as the key determinant of cell mechanics in response to ECM cues.

2017-05-17 | E-MTAB-5217 | biostudies-arrayexpress

YAP-TEAD multiphasic activation regulates pluripotent stem cell mechanics to drive cardiac specification and contractility in pathological heart.

Project description:YAP transcriptional regulator controls cell mechanics by activating genes involved in cell-matrix interaction following extracellular matrix (ECM) remodelling and stiffening. YAP is needed for cardiogenesis in mouse but is repressed in adult cardiomyocytes. The protein is reactivated following ischemic insults, although the timing and mechanisms underlying YAP depletion during heart development and the reason for its reactivation are unclear. Here, we combine pluripotent stem cell (PSC) cardiac differentiation, mouse embryo development and human heart tissue analysis to demonstrate that the fine-tuning of cell mechanics, as controlled by YAP multiphasic activation through TEAD transcription, is crucial for mesoderm commitment and cardiac progenitor specification. Finally, by adopting induced PSC models of dilated cardiomyopathy, we prove that YAP-TEAD reactivation in diseased cardiomyocytes empowers calcium handling apparatus and increases cell contractility. Given YAP prompt activation following myocardial infarction, we unveil a novel role for mechanosensing in connecting ECM remodelling to cardiomyocyte function in pathological heart.

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Project description:While cell mechanics and metastatic potential are related, the molecular factors that drive these behaviors remain unknown. Understanding how molecular signaling networks modulate cellular phenotype and mechanotype can help elucidate how metastasis occurs. Therefore, we developed a workflow to measure mechanical properties and gene expression on the single cell level. The process combines atomic force microscopy and optical microscopy to measure the mechanics and morphology of individual ovarian cancer cells, followed by multiplexed RT-qPCR gene expression analysis. Surprisingly, the genes that most strongly correlated with mechanical properties were not cytoskeletal, but rather were markers of epithelial-to-mesenchymal transition and cancer stemness. A dimensionality reduction analysis showed that cells of different metastatic potential were best identified through combining mechanical and gene expression data. Finally, a network analysis revealed master regulators that can predictably stiffen and soften cells while modulating cell migration. The single cell genomechanics methods demonstrate how molecular drivers can disable biophysical processes underpinning metastasis.

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