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Disrupting Mechanotransduction Promotes Regenerative Phenotypes in Human Cells

ABSTRACT: Disrupting Mechanotransduction Promotes Regenerative Phenotypes in Human Cells

PROVIDER: PRJNA704343 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13770935.fastq.gz	Fastqsanger.gz
	SRR13770936.fastq.gz	Fastqsanger.gz
	SRR13770937.fastq.gz	Fastqsanger.gz
	SRR13770938.fastq.gz	Fastqsanger.gz
	SRR13770939.fastq.gz	Fastqsanger.gz

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Disrupting Mechanotransduction Promotes Regenerative Phenotypes in Human Cells

Project description:We quantify the effects of FAK inhibition on three-dimensional (3D) cultured human fibroblasts at the cellular and transcriptomic level using single cell RNA-sequencing. We demonstrate that mechanical stress induces pro-fibrotic fibroblast differentiation fates in large organisms, which can effectively be averted by FAK inhibition, which induces discrete fibroblast clusters that promote wound regeneration.

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Disrupting Mechanotransduction Decreases Fibrosis and Contracture in Porcine Split Thickness Skin Grafting

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Mechanotransduction regulates adipose estrogen output and its impact on tumor cell growth

Project description:Adipose stromal cells (ASCs) are the primary source of local estrogens in adipose tissue, aberrant production of which promotes estrogen receptor-positive (ER+) breast cancer. Here we show that extracellular matrix (ECM) rigidity and cell contractility are two opposing determinants for estrogen output of ASCs. Using synthetic ECMs and elastomeric micropost arrays with tunable rigidity, we find that increasing matrix compliance induces transcription of aromatase, a rate-limiting enzyme in estrogen biosynthesis. This mechanical cue is transduced sequentially by Discoidin Domain Receptor 1 (DDR1), c-Jun N-terminal kinase 1 (JNK1), and phosphorylated JunB, which binds to and activates two breast cancer-associated aromatase promoters. In contrast, elevated cell contractility due to actin stress fiber formation dampens aromatase transcription. Mechanically stimulated stromal estrogen production enhances estrogen-dependent transcription in ER+ tumor cells and promotes their growth. This novel mechanotransduction pathway underlies communications between ECM, stromal hormone output, and cancer cell growth within the same microenvironment. Total RNA was isolated from primary adipose stromal cells after 2d culture or 3d Collagen gel for 21 hours. Triplicates for each conditioned were analyzed

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Disrupting Mechanotransduction Decreases Fibrosis and Contracture in Porcine Split Thickness Skin Grafting

Project description:We quantify the effects of FAK inhibition on porcine cells at the cellular and transcriptomic level using single-cell RNA-sequencing. We characterize fibrotic porcine dermal cells and compare them to regenerative cells and also unwounded tissue.

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Project description:Tissue-scale architecture and mechanical properties instruct cell behavior in physiological and diseased conditions, but our understanding of the underlying mechanisms remains fragmentary. Here we show that ECM stiffness, spatial confinements, and applied forces including stretching of the mouse skin regulate mitochondrial dynamics. Actomyosin tension promotes phosphorylation of MIEF1, limiting the recruitment of DRP1 at mitochondria, peri-mitochondrial F-actin formation, and mitochondrial fission. Strikingly, mitochondrial fission is also a general mechanotransduction mechanism. Indeed we found that DRP1- and MIEF1-dependent fission is required and sufficient to regulate three transcription factors of broad relevance such as YAP-TAZ, SREBP1-2, and NRF2 to control cell proliferation, lipogenesis, antioxidant metabolism, chemotherapy resistance, and adipocyte differentiation in response to mechanical cues. This extends to the mouse liver, where DRP1 regulates hepatocyte proliferation and identity, hallmark YAP-dependent phenotypes. We propose that mitochondria fulfill a unifying signaling function by which the mechanical tissue microenvironment coordinates complementary cell functions.

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