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Piezo1 dictates K⁺ homeostasis through coordinated regulation of the ubiquitin ligase Kelch-like 3 in RBCs and the kidney

ABSTRACT: The maintenance of potassium (K+) balance is a fundamental biological process involving multiple organs. However, mechanisms by which inter-organ communication regulates K+ homeostasis remain largely unexplored. By combining human genetics and mouse model generation using CRIPSR/Cas9, we demonstrate that the ubiquitin ligase Kelch-like 3 (KLHL3) orchestrates K⁺ transport across K⁺-storing erythrocytes and K⁺-excreting kidneys by interacting with the mechanosensitive Ca2+ channel Piezo1.

ORGANISM(S): Mus musculus

PROVIDER: GSE294294 | GEO | 2026/01/01

REPOSITORIES: GEO

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Piezo1 dictates K⁺ homeostasis through coordinated regulation of the ubiquitin ligase Kelch-like 3 in RBCs and the kidney

Project description:Piezo1 dictates K⁺ homeostasis through coordinated regulation of the ubiquitin ligase Kelch-like 3 in RBCs and the kidney

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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.

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Project description:Piezo1 is a mechanosensitive ion channel that has gained recognition for its role in regulating diverse physiological processes. However, the influence of Piezo1 in inflammatory disease, including infection and tumor-immunity, is not well-studied. We postulated that Piezo1 links physical forces to immune regulation in myeloid cells. We discovered signal transduction via Piezo1 in myeloid cells and established this channel as the primary sensor of mechanical stress in these cells. Global inhibition of Piezo1 was protective against both cancer and septic shock and resulted in a diminution in suppressive myeloid cells. Moreover, deletion of Piezo1 in myeloid cells protected against cancer and increased survival in poly-microbial sepsis. Mechanistically, we show that mechanical stimulation promotes Piezo1-dependent myeloid cell expansion by suppressing Rb. We further show Piezo1-mediated silencing of Rb is regulated via upregulation of HDAC2. Collectively, our work uncovers Piezo1 as a targetable immune checkpoint that drives immune-suppressive myelopoiesis in cancer and infectious disease.

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

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

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.

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