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Mechanotransduction mediated by cyclical respiratory motion maintains lung alveolar epithelial cell fate

ABSTRACT: Mechanotransduction mediated by cyclical respiratory motion maintains lung alveolar epithelial cell fate

PROVIDER: PRJNA835452 | ENA |

REPOSITORIES: ENA

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Mechanotransduction mediated by cyclical respiratory motion maintains lung alveolar epithelial cell fate

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FAK is required for suppressing aberrant nuclear mechanotransduction and DNA methylation to prevent vascular injury

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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Project description:PAthway representing mechanotransduction

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Interleukin-11 causes alveolar type 2 cell dysfunction and prevents alveolar regeneration [RNA-seq]

Project description:Following lung injury, alveolar regeneration is characterized by the transformation of alveolar type 2 (AT2) cells, via a transitional KRT8+ state, into alveolar type 1 (AT1) cells. In lung disease, dysfunctional intermediate cells accumulate, AT1 cells are diminished and fibrosis occurs. Using single cell RNA sequencing datasets of human interstitial lung disease, we found that interleukin-11 (IL11) is specifically expressed in aberrant KRT8 expressing KRT5-/KRT17+ and basaloid cells. Stimulation of AT2 cells with IL11 or TGFβ1 caused EMT, induced KRT8+ and stalled AT1 differentiation, with TGFβ1 effects being IL11 dependent. In bleomycin injured mouse lung, IL11 was increased in AT2-derived KRT8+ cells and deletion of Il11ra1 in lineage labeled AT2 cells reduced KRT8+ expression, enhanced AT1 differentiation and promoted alveolar regeneration, which was replicated in therapeutic studies using anti-IL11. These data show that IL11 maintains AT2 cells in a dysfunctional transitional state, impairs AT1 differentiation and blocks alveolar regeneration across species.

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UBE2A/B is the trans-acting factor mediating mechanotransduction and contact inhibition

Project description:Mechanotransduction converts mechanical stimuli into biochemical signals to regulate cell growth, differentiation, and survival. However, how mechanotransduction is linked to gene expression remains poorly understood. Here, we report the identification of UBE2A as an mechano-sensitive trans-acting factor, which translocates from the cytosol to the nucleus upon mechanical stimuli. UBE2A is an E2 enzyme that catalyzes ubiquitination of histone, which eventually results in transcription activation of downstream genes. Using ChIP-seq and RNAseq analysis, we identify downstream genes of UBE2A, including YAP1, a well-known mechanotransducer. Knock-down of UBE2A/B significantly downregulates YAP1 protein expression. Our findings identify the new mechanotransduction pathway that regulates gene expression through histone ubiquitination by UBE2A/B.

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