Piezo1 activation induces fibronectin reduction and PGF2α secretion via arachidonic acid cascade

Morozumi, Wataru; Aoshima, Kota; Inagaki, Satoshi; Iwata, Yuji; Takagi, Yuya; Nakamura, Shinsuke; Hara, Hideaki; Shimazawa, Masamitsu

doi:10.1016/j.exer.2021.108917

Cited by 13 publications

(12 citation statements)

References 28 publications

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“…On the other hand, the data indicated that PIEZO1 knockdown reduced the levels of fibronectin and collagen I in immortalized mouse renal SV40‐MES‐13 cells and in animal model of renal fibrosis induced by unilateral ureteral obstruction (Fu et al, 2021). At the same time, selective agonist‐induced PIEZO1 activity (by small molecule Yoda1) led to reduced expression level of fibronectin in human trabecular meshwork cells (Morozumi et al, 2022). Taken together, the regulation of PIEZO1 by the components of ECM/cytoskeleton highlights the importance of these structures in the control of PIEZO1 functioning.…”

Section: Regulation Of Piezo1 By Ecm and Cytoskeletal Proteinsmentioning

confidence: 99%

“…The ECM is a complex network of different proteins, growth factors and other macromolecules, which is constantly self-renewing and remodeling through protein synthesis and degradation (Cox & Erler, 2011). The ECM is a highly dynamic system that controls (Morozumi et al, 2022). Taken together, the regulation of PIEZO1 by the components of ECM/cytoskeleton highlights the importance of these structures in the control of PIEZO1 functioning.…”

Section: Ecm Proteinsmentioning

confidence: 99%

“…Among the PIEZO family, PIEZO1 is studied in more detail, compared to PIEZO2. It was shown that Ca 2+ influx through PIEZO1 could regulate the activity of numerous Ca 2+ ‐dependent molecules, for example (but not limited to), calcium‐activated potassium (KCa) channels (Chubinskiy‐Nadezhdin et al, 2017, 2019, 2020; Jakob et al, 2021) and signaling pathways, including calpain‐ or arachidonic acid cascades (Aglialoro et al, 2020; Morozumi et al, 2022; Zhao et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of PIEZO1 channels by lipids and the structural components of extracellular matrix/cell cytoskeleton

Vasileva

Chubinskiy-Nadezhdin

2023

Journal Cellular Physiology

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PIEZO1 is a mechanosensitive channel widely presented in eukaryotic organisms. Although the PIEZO family was discovered in 2010, main questions related to the molecular structure as well as to specific activation mechanisms and regulating pathways remain open. Two hypotheses of PIEZO1 gating were formulated: the first, as a dominant hypothesis, through the plasma membrane (force‐from‐lipids) and the second, via the participation of the cytoskeleton and the components of the extracellular matrix (ECM) (force‐from‐filaments). Many researchers provide convincing evidence for both hypotheses. It was demonstrated that PIEZO1 has a propeller‐like shape forming a membrane curvature within the lipid bilayer. That suggests the participation of lipids in channel modulation, and many studies demonstrate the critical role of lipids and compounds that modify the lipid bilayer in the regulation of PIEZO1 properties. At the same time, the components of ECM and cortical cytoskeleton can be affected by the membrane curvature and thus have an impact on PIEZO1 properties. In living cells, PIEZO1 properties are reported to be critically dependent on channel microenvironment that is on combinatorial influence of plasma membrane, cytoskeleton and ECM. Thus, it is necessary to understand which factors can affect PIEZO1 and consider them when interpreting the role of PIEZO1 in various physiological processes. This review summarizes the current knowledge about regulation of Piezo1 by lipids and the components of ECM and cytoskeleton.

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Section: Regulation Of Piezo1 By Ecm and Cytoskeletal Proteinsmentioning

confidence: 99%

Section: Ecm Proteinsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of PIEZO1 channels by lipids and the structural components of extracellular matrix/cell cytoskeleton

Vasileva

Chubinskiy-Nadezhdin

2023

Journal Cellular Physiology

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“…Cationic mechanosensitive channels (CMCs), including transient receptor potential cation channel subfamily V member 4 (TRPV4) ( Ryskamp et al, 2016 ), TWIK-related potassium channel-1 (TREK-1) ( Carreon et al, 2017 ), and Piezo ( Yarishkin et al, 2021 ; Zhu et al, 2021 ; Morozumi et al, 2022 ), have the potential to modulate calcium homeostasis, cell cytoskeleton organization, extracellular matrix (ECM) composition, and PGF2alpha secretion, and could therefore influence the responses of TM cells. In accordance with Yarishkin et al, we also found that GsMTx4, a non-selective inhibitor of CMCs, reduces the TM’s steady-state facility of AH outflow ( Yarishkin et al, 2021 ; Zhu et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Cationic Mechanosensitive Channels Mediate Trabecular Meshwork Responses to Cyclic Mechanical Stretch

et al. 2022

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The trabecular meshwork (TM) is responsible for intraocular pressure (IOP) homeostasis in the eye. The tissue senses IOP fluctuations and dynamically adapts to the mechanical changes to either increase or decrease aqueous humor outflow. Cationic mechanosensitive channels (CMCs) have been reported to play critical roles in mediating the TM responses to mechanical forces. However, how CMCs influence TM cellular function affect aqueous humor drainage is still elusive. In this study, human TM (HTM) cells were collected from a Chinese donor and subjected to cyclically equiaxial stretching with an amplitude of 20% at 1 Hz GsMTx4, a non-selective inhibitor for CMCs, was added to investigate the proteomic changes induced by CMCs in response to mechanical stretch of HTM. Gene ontology enrichment analysis demonstrated that inhibition of CMCs significantly influenced several biochemical pathways, including store-operated calcium channel activity, microtubule cytoskeleton polarity, toll-like receptor signaling pathway, and neuron cell fate specification. Through heatmap analysis, we grouped 148 differentially expressed proteins (DEPs) into 21 clusters and focused on four specific patterns associated with Ca2+ homeostasis, autophagy, cell cycle, and cell fate. Our results indicated that they might be the critical downstream signals of CMCs adapting to mechanical forces and mediating AH outflow.

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“…Cationic mechanosensitive channels (CMCs), including transient receptor potential cation channel subfamily V member 4 (TRPV4) (Ryskamp et al, 2016), TWIK-related potassium channel-1 (TREK-1) (Carreon et al, 2017), and Piezo (Yarishkin et al, 2021;Zhu et al, 2021;Morozumi et al, 2022), have the potential to modulate calcium homeostasis, cell cytoskeleton organization, extracellular matrix (ECM) composition, and PGF2alpha secretion, and could therefore influence the responses of TM cells. In accordance with Yarishkin et al, we also found that GsMTx4, a non-selective inhibitor of CMCs, reduces the TM's steady-state facility of AH outflow (Yarishkin et al, 2021;Zhu et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

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Piezo1 activation induces fibronectin reduction and PGF2α secretion via arachidonic acid cascade

Cited by 13 publications

References 28 publications

Regulation of PIEZO1 channels by lipids and the structural components of extracellular matrix/cell cytoskeleton

Regulation of PIEZO1 channels by lipids and the structural components of extracellular matrix/cell cytoskeleton

Cationic Mechanosensitive Channels Mediate Trabecular Meshwork Responses to Cyclic Mechanical Stretch

Table1.docx

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