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Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity

ABSTRACT: Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity

PROVIDER: PRJNA1165661 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30805568_1.fastq.gz	Fastqsanger.gz
	SRR30805568_2.fastq.gz	Fastqsanger.gz
	SRR30805569_1.fastq.gz	Fastqsanger.gz
	SRR30805569_2.fastq.gz	Fastqsanger.gz
	SRR30805570_1.fastq.gz	Fastqsanger.gz

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Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity [II]

Project description:Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity [II]

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Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity

Project description:Group-2 innate-lymphoid cells (ILC2s) are critical mediators of the type-2 immune responses in multiple lung pathologies. We show that Piezo1, a mechanosensitive ion channel, plays a key role in regulating ILC2 functions by linking mechanical cues to biochemical signaling pathways. Both murine and human ILC2s strongly express Piezo1, and its activation by Yoda1 selectively enhances IL-13 production through calcium influx, which activates the mTOR-S6K pathway. This pathway leads to translational reprogramming, favoring IL-13 translation. Piezo1-deficient in ILC2s impairs this process, reducing IL-13 levels and resulting in attenuated lung inflammation and fibrosis in mouse models of IL-33- or Alternaria alternata-induced airway inflammation and bleomycin-induced fibrosis. These findings position Piezo1 as a critical mediator of ILC2-driven type-2 immune responses and highlight its potential as a therapeutic target for lung diseases characterized by excessive inflammation. This streamlined understanding of Piezo1 function improves focus on its mechanistic role in lung pathology.

2024-09-30 | GSE278085 | GEO

Piezo1-mediated Mechanotransduction Shapes ILC2 Translational Activity, Functions, and Lung Pathogenicity [II]

2025-07-15 | GSE279338 | GEO

Role of Piezo1-mediated mechanotransduction in osteocyte differentiation

Project description:Mechanical force is a fundamental regulator of bone development and homeostasis. Mechanosensitive osteocytes are the most abundant bone cells that form interconnected dendrites to respond to mechanical stimuli and interact with the bone-forming osteoblasts and the bone-remodeling osteoclasts. However, the molecular mechanisms underlying osteocyte maturation and dendrite formation remain unclear. By generating a Piezo1 "knock-out" osteocyte cell line, we identified a key role of Piezo1-mediated mechanotransduction in osteocyte differentiation. QRT-PCR analysis revealed delayed osteocyte differentiation in the Piezo1 KO cells relative to WT cells. By performing bulk RNA sequencing of WT and Piezo1 KO OCY454 cells at early (D1), intermediate (D14), and late (D28) stages of differentiation allowed for the identification of key signaling pathways in driving normal osteocyte dfiferentiation, as well as those regulated by Piezo1 mechanotransduction.

2024-09-20 | GSE277264 | GEO

Role of Piezo1-mediated mechanotransduction in osteocyte differentiation

Project description:Role of Piezo1-mediated mechanotransduction in osteocyte differentiation

| PRJNA1161617 | ENA

Piezo1 channels restrain ILC2s and regulate the development of airway hyperactivity [yoda1]

Project description:Mechanosensitive ion channels sense force and pressure in immune cells to drive the inflammatory response in highly mechanical organs. Here we report that Piezo1 channels repress group 2 innate lymphoid cells (ILC2s)-driven type 2 inflammation in the lungs. Piezo1 is induced on lung ILC2s upon activation, as genetic ablation of Piezo1 in ILC2s increases their function and exacerbates the development of airway hyperreactivity (AHR). Conversely, Piezo1 agonist Yoda1 reduces ILC2-driven lung inflammation. Mechanistically, Yoda1 inhibits ILC2 cytokine secretion and proliferation in a KLF2-dependent manner, as we further found that Piezo1 engagement reduces ILC2 oxidative metabolism. Consequently, in vivo Yoda1 treatment notably reduces the development of AHR in experimental models of ILC2-driven allergic asthma. Human circulating ILC2s express and induce Piezo1 upon activation, as Yoda1 treatment of humanized mice reduces human ILC2-driven AHR. Our studies define Piezo1 as a critical regulator of ILC2s and we propose the potential of Piezo1 activation as a novel therapeutic approach for the treatment of ILC2-driven allergic asthma.

2024-02-20 | GSE255881 | GEO

Piezo1 channels restrain ILC2s and regulate the development of airway hyperactivity [piezo1KO]

2024-02-20 | GSE255882 | GEO

RNA-seq of wildtype and PIEZO1 knockout mice livers to investigate lipid and glucose regulation by the endothelial force sensor PIEZO1

Project description:PIEZO1 is a mechanically-activated ion channel that contributes to flow sensing in vascular endothelium. Moreover, deletion of endothelial PIEZO1 was recently found to suppress activation of Notch1 target genes in hepatic microvascular endothelium. Here, because of the liver’s dominant role in lipid regulation, we set out to test the novel hypothesis that endothelial PIEZO1 regulates hepatic lipid homeostasis. We performed bulk RNA sequencing on PIEZO1-deleted mice exposed to chow and high fat diets. Our transcriptomics analysis reveal unexpected relevance to lipid and glucose homeostasis.

2024-06-29 | E-MTAB-9996 | biostudies-arrayexpress

RNA-sequencing of wild type and Piezo1-Cko mice under sham or TAC surgery

Project description:Mechanotransduction has been lately recognized as a major regulator of organ homeostasis under a myriad of pathological conditions. The role of Piezo1 in cardiac hypertrophy has never been explored. Here we performed RNA-Seq assay for wild type and Piezo1-Cko mice under sham or TAC surgery.

2024-01-01 | GSE179107 | GEO

Piezo1 initiates host immune defense against pathogenic fungi through mechanosensory recognition of Candida albicans hyphae

Project description:Candida albicans metamorphoses from benign yeast to a rigid hyphae , becoming an opportunistic pathogen in immunocompromised patients. The process by which immune cells discern fungal transformations remains elusive. Here we report that the mechanosensitive ion channel Piezo1 is indispensable for recognizing fungal hyphae and triggering anti-fungal innate immune responses. Hyphae-triggered Piezo1 activation increased CLRs expression in innate immune cells by inducing the expression of C/EBPb via the Piezo1/CaMKs/CREB axis. In addition, Piezo1/CaMKs signaling activated kinases NDR1/2, which augmented NLRP3 inflammasome assembly and promoted hyphae-induced inflammation. Abolishing the yeast-to-hyphae transition dampens CLR and NLRP3 activation. Piezo1-deficient mice exhibit compromised clearance of C. albicans infection, whereas Piezo1 agonist amplifies C. albicans clearance. In addition, CaMKs, CREB or NDR1/2 inhibition exacerbates hyphae infections, like Piezo1 deficiency. Therefore, we ascertain Piezo1-mediated mechanotransduction as vital for immune surveillance and control of hyphal C. albicans, heralding Piezo1 agonist as a potential remedy for fungal infections.

2025-05-22 | GSE279850 | GEO

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