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

ABSTRACT: 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.

ORGANISM(S): Sus scrofa

PROVIDER: GSE190849 | GEO | 2021/12/16

REPOSITORIES: GEO

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

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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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Tension sensing by FAK governs nuclear mechanotransduction, trancriptome and fate endothelial transcriptome and fate

Project description:Endothelial cell (EC) attachment to the matrix and adjacent cells generates a mechanical environment that maintains a restrictive barrier against the uncontrolled influx of circulating protein and immune cells. Mechanisms that mediate the transition from restrictive to leaky endothelium, a hallmark of tissue injury exemplified by acute lung injury (ALI), remain elusive. Here, we show that FAK sensing and transmission of mechanical tension to the EC nucleus governs cell fate. In FAK-deleted EC, increased EC tension activated DNMT3a, which induced methylation of the KLF2 promoter leading to impaired synthesis of KLF2 and restrictive EC transcriptome, including S1PR1. FAK suppressed DNMT3a activity by restricting the tyrosine phosphorylation of nuclear envelope protein, emerin at Y74/Y95, and its localization in a nuclear cap. Inhibiting emerin phosphorylation or DNMT3a activity in damaged lungs enabled KLF2 transcription of S1PR1, rescuing the restrictive EC phenotype. Our works reveal a paradigm whereby FAK sensing of tension transmission to the nucleus maintains restrictive EC transcriptome and lung homeostasis.

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Project description:Mechanical forces generated through adhesive interaction of endothelial cells (EC) influence nuclear envelope and thereby gene transcription. Alteration in EC mechanical forces may trigger aberrant gene transcription leading to lethal vascular diseases including acute lung injury (ALI). The intrinsic pathways that instruct EC nuclear-mechanotransduction and thereby maintains vascular homeostasis remain elusive. We have identified focal adhesion kinase (FAK)-mediated mechanotransduction at the nuclear envelope in instructing transcription of EC-barrier protective genes. We show that loss of EC-FAK increases intracellular tension, which in turn activates nuclear envelop protein emerin, and DNA methyltransferase 3a (DNMT3a). Methylation of transcription factor KLF2 promoter by DNMT3a impaired KLF2 synthesis and transcription of the crucial barrier-maintaining gene, S1PR1. Restoring KLF2 or S1PR1 expression or impairing emerin or DNMT3a activity rescued vascular homeostasis in lungs with FAK-deficient or WT-damaged endothelium. Thus, FAK protects against tension-induced aberrant DNA methylation in EC and is a promising target to prevent ALI.

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The porcine microRNA transcriptome response to porcine cytomegalovirus infection

Project description:Porcine cytomegalovirus (PCMV; genus Cytomegalovirus, subfamily Betaherpesvirinae, family Herpesviridae) is an immunosuppressive virus that mainly inhibits the immune function of T lymphocytes and macrophages, which has caused great distress to the farming industry. In this study, we obtained the miRNA expression profiles of PCMV-infected and control porcine macrophages, PCMV-infected and control porcine tissues via high-throughput sequencing. The comprehensive analysis of miRNA profiles showed that 306 miRNA database annotated and 295 novel pig-encoded miRNAs were detected. Gene Ontology (GO) analysis of the target genes of miRNAs in PCMV infected porcine macrophages showed that the differentially expressed miRNAs are mainly involved in immune and metabolic process. This is the first report of the miRNA transcriptome in PCMV infected porcine macrophages and PCMV infected tissues and the analysis of the miRNA regulatory mechanism during PCMV infection. Further research into the regulatory mechanisms of miRNAs during immunosuppressive viral infections will contribute to the treatment and prevention of immunosuppressive viruses.

2015-12-19 | GSE76156 | GEO

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