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Futers, S.

Publications and source records attributed to Futers, S..

3 recordsLinked to original sources

Contribution of endothelial Piezo1 in mechanically induced muscle hypertrophy

Piezo1 proteins form nonselective cation channels with key roles in endothelial responses to mechanical forces. Here we reveal that endothelial Piezo1 regulates skeletal muscle hypertrophy following mechanical overload. Using a conditional endothelial cell-specific deletion of Piezo1 in adult mice, we assessed the role of endothelial Piezo1 in mechanical overload-induced muscle hypertrophy in the extensor digitorum longus. Endothelial Piezo1 deletion blunted muscle hypertrophy following mechanical overload despite normal baseline vascularisation, as evidenced by a lack of increase in muscle mass and abolished myofibre growth. Despite being required for optimal muscle growth, endothelial Piezo1 was dispensable for muscle regeneration after injury. In line with this, the reduced muscle growth following mechanical overload was not associated with impaired myonuclear accretion. We suggest that endothelial Piezo1 participates in a myofibre partnership that regulates skeletal muscle growth in response to mechanical overload.

physiology↗

PIEZO1 force sensing controls global lipid homeostasis

How cardiovascular activity beneficially regulates lipid homeostasis is unclear. Here we hypothesise a mechanism in which mechanical force sensed by PIEZO1 ion channels in endothelium links blood flow to lipid regulation. We engineered mice for conditional deletion of PIEZO1 in endothelium and determined consequences for lipid regulation. Prominent are upregulated expression of hepatic Cyp7a1 and intestinal Ldlr genes, which are pivotal in cholesterol catabolism and excretion. Consistent with such regulation is endothelial PIEZO1-dependence of hepatic, intestinal and whole body cholesterol and bile homeostasis. There is organ perfusion-dependent gene regulation via endothelial PIEZO1 and downstream nitric oxide synthase. Endothelial PIEZO1-deleted mice are protected against hyperlipidaemia and ectopic fat deposition. Human PIEZO1 gene variants and a recapitulated human PIEZO1 gain-of-function variant in mice associate with dyslipidaemia. The data suggest lipid-promoting effects of endothelial force sensing and new opportunity for understanding and addressing problems of hyperlipidaemia.

physiology↗

Piezo1 channel activates ADAM10 sheddase to regulate Notch1 and gene expression

Mechanical force has emerged as a determinant of Notch signalling but the mechanisms of force sensing and coupling to Notch are unclear. Here we propose a role for Piezo1 channels, the recently identified mechanosensors of mammalian systems. Piezo1 channel opening in response to shear stress or a chemical agonist led to activation of a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10), a Ca2+-regulated transmembrane sheddase that mediates S2 Notch1 cleavage. Consistent with this observation there was increased Notch1 intracellular domain (NICD) that depended on ADAM10 and the downstream S3 cleavage enzyme, {gamma}-secretase. Endothelial-specific disruption of Piezo1 in mice led to decreased Notch1-regulated gene expression in hepatic vasculature, consistent with prior evidence that Notch1 controls hepatic perfusion. The data suggest Piezo1 as a mechanism for coupling physiological force at the endothelium to ADAM10, Notch1, gene expression and vascular function.

cell biology↗