scholarly journals Role of mechanosensitive ion channels in cell signaling

1997 ◽  
Vol 73 ◽  
pp. 23
Author(s):  
Masahiro Sokabe
Keyword(s):  
Ion Channels ◽  
Cell Signaling ◽  
Mechanosensitive Ion Channels

scholarly journals Mechanical activation of epithelial Na+ channel relies on an interdependent activity of the extracellular matrix and extracellular N-glycans of αENaC

2017 ◽  
Author(s):  
Fenja Knoepp ◽  
Zoe Ashley ◽  
Daniel Barth ◽  
Marina Kazantseva ◽  
Pawel P. Szczesniak ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Ion Channels ◽  
Shear Force ◽  
Na Channel ◽  
Pressure Regulation ◽  
Mechanical Environment ◽  
Mechanosensitive Ion Channels ◽  
Glycosylation Sites ◽  
Epithelial Na Channel

AbstractMechanotransduction describes how cells perceive their mechanical environment and mechanosensitive ion channels are important for this process. ENaC (epithelial Na+ channel)/DEG (degenerin) proteins form mechanosensitive ion channels and it is hypothesized their interaction with the extracellular matrix (ECM) via ‘tethers’ is required for mechanotransduction. Channels formed by vertebrate α, β and γ ENaC proteins are activated by shear force (SF) and mediate electrolyte/fluid-homeostasis and blood pressure regulation. Here, we report an interdependent activity of ENaC and the ECM that mediates SF effects in murine arteries and heterologously expressed channels. Furthermore, replacement of conserved extracellular N-glycosylated asparagines of αENaC decreased the SF response indicating that the attached N-glycans provide a connection to the ECM. Insertion of N-glycosylation sites into a channel subunit, innately lacking these motifs, increased its SF response. These experiments confirm an interdependent channel/ECM activity of mechanosensitive ENaC channel and highlight the role of channel N-glycans as new constituents for the translation of mechanical force into cellular signals.

scholarly journals Channelling the Force to Reprogram the Matrix: Mechanosensitive Ion Channels in Cardiac Fibroblasts

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 990
Author(s):  
Leander Stewart ◽  
Neil A. Turner
Keyword(s):  
Ion Channels ◽  
Myocardial Function ◽  
Current Knowledge ◽  
Cardiac Fibroblasts ◽  
Heart Tissue ◽  
Cardiac Remodelling ◽  
Paracrine Signalling ◽  
Mechanosensitive Ion Channels ◽  
The Matrix

Cardiac fibroblasts (CF) play a pivotal role in preserving myocardial function and integrity of the heart tissue after injury, but also contribute to future susceptibility to heart failure. CF sense changes to the cardiac environment through chemical and mechanical cues that trigger changes in cellular function. In recent years, mechanosensitive ion channels have been implicated as key modulators of a range of CF functions that are important to fibrotic cardiac remodelling, including cell proliferation, myofibroblast differentiation, extracellular matrix turnover and paracrine signalling. To date, seven mechanosensitive ion channels are known to be functional in CF: the cation non-selective channels TRPC6, TRPM7, TRPV1, TRPV4 and Piezo1, and the potassium-selective channels TREK-1 and KATP. This review will outline current knowledge of these mechanosensitive ion channels in CF, discuss evidence of the mechanosensitivity of each channel, and detail the role that each channel plays in cardiac remodelling. By better understanding the role of mechanosensitive ion channels in CF, it is hoped that therapies may be developed for reducing pathological cardiac remodelling.

scholarly journals Ion Channels in Epithelial Dynamics and Morphogenesis

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2280
Author(s):  
Ankit Roy Choudhury ◽  
Jörg Großhans ◽  
Deqing Kong
Keyword(s):  
Nervous System ◽  
Ion Channels ◽  
Epithelial Cells ◽  
Cell Types ◽  
Mechanical Forces ◽  
Morphogenetic Movements ◽  
Mechanosensitive Ion Channels ◽  
Channel Proteins ◽  
Epithelial Tissues

Mechanosensitive ion channels mediate the neuronal sensation of mechanical signals such as sound, touch, and pain. Recent studies point to a function of these channel proteins in cell types and tissues in addition to the nervous system, such as epithelia, where they have been little studied, and their role has remained elusive. Dynamic epithelia are intrinsically exposed to mechanical forces. A response to pull and push is assumed to constitute an essential part of morphogenetic movements of epithelial tissues, for example. Mechano-gated channels may participate in sensing and responding to such forces. In this review, focusing on Drosophila, we highlight recent results that will guide further investigations concerned with the mechanistic role of these ion channels in epithelial cells.

scholarly journals A population of gut epithelial enterochromaffin cells is mechanosensitive and requires Piezo2 to convert force into serotonin release

2018 ◽  
Vol 115 (32) ◽  
pp. E7632-E7641 ◽  
Author(s):  
Constanza Alcaino ◽  
Kaitlyn R. Knutson ◽  
Anthony J. Treichel ◽  
Gulcan Yildiz ◽  
Peter R. Strege ◽  
...  
Keyword(s):  
Ion Channels ◽  
Molecular Mechanism ◽  
Ionic Current ◽  
Serotonin Release ◽  
Lineage Tracing ◽  
Conditional Knockout ◽  
Intestinal Epithelial ◽  
Mechanosensitive Ion Channels ◽  
Ec Cells

Enterochromaffin (EC) cells constitute the largest population of intestinal epithelial enteroendocrine (EE) cells. EC cells are proposed to be specialized mechanosensory cells that release serotonin in response to epithelial forces, and thereby regulate intestinal fluid secretion. However, it is unknown whether EE and EC cells are directly mechanosensitive, and if so, what the molecular mechanism of their mechanosensitivity is. Consequently, the role of EE and EC cells in gastrointestinal mechanobiology is unclear. Piezo2 mechanosensitive ion channels are important for some specialized epithelial mechanosensors, and they are expressed in mouse and human EC cells. Here, we use EC and EE cell lineage tracing in multiple mouse models to show that Piezo2 is expressed in a subset of murine EE and EC cells, and it is distributed near serotonin vesicles by superresolution microscopy. Mechanical stimulation of a subset of isolated EE cells leads to a rapid inward ionic current, which is diminished by Piezo2 knockdown and channel inhibitors. In these mechanosensitive EE cells force leads to Piezo2-dependent intracellular Ca2+increase in isolated cells as well as in EE cells within intestinal organoids, and Piezo2-dependent mechanosensitive serotonin release in EC cells. Conditional knockout of intestinal epithelial Piezo2 results in a significant decrease in mechanically stimulated epithelial secretion. This study shows that a subset of primary EE and EC cells is mechanosensitive, uncovers Piezo2 as their primary mechanotransducer, defines the molecular mechanism of their mechanotransduction and mechanosensitive serotonin release, and establishes the role of epithelial Piezo2 mechanosensitive ion channels in regulation of intestinal physiology.

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