The potential role of mechanosensitive ion channels in substrate stiffness-regulated Ca2+ response in chondrocytes

2021 ◽  
pp. 1-10
Author(s):  
Genlai Du ◽  
Weiyi Chen ◽  
Li Li ◽  
Quanyou Zhang
Keyword(s):  
Ion Channels ◽  
Potential Role ◽  
Substrate Stiffness ◽  
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.

Sa1719 Potential Role of Acid Sensitive Ion Channels and 5-Hydroxytryptamine Receptors in a Rat Model of Refux Esophagitis

2016 ◽  
Vol 150 (4) ◽  
pp. S356
Author(s):  
Anastasia Shcherbakova ◽  
Heba Abdel-Aziz ◽  
Olaf Kelber ◽  
Gudrun Ulrich-Merzenich
Keyword(s):  
Ion Channels ◽  
Rat Model ◽  
Potential Role ◽  
Hydroxytryptamine Receptors

The Potential Role of Nerve Growth Factor (NGF) in Painful Neuromas and the Mechanism of Pain Relief by their Relocation to Muscle

2006 ◽  
Vol 31 (6) ◽  
pp. 652-656 ◽  
Author(s):  
D. D. ATHERTON ◽  
O. TAHERZADEH ◽  
P. FACER ◽  
D. ELLIOT ◽  
P. ANAND
Keyword(s):  
Nerve Growth Factor ◽  
Ion Channels ◽  
Growth Factor ◽  
Pain Relief ◽  
Sensory Neurons ◽  
Surgical Procedures ◽  
Potential Role ◽  
Nerve Growth ◽  
Pain Transmission

Painful neuromas have been successfully treated by surgical procedures including relocation to muscle, but the underlying molecular mechanism remains unclear. Nerve growth factor (NGF) is secreted by tissues and promotes the expression of ion channels and neuropeptides in sensory neurons involved in pain transmission. We hypothesised that excess of NGF may lead to pain in neuromas and that the efficacy of surgical relocation results from deprivation of NGF, i.e. translocation from NGF-rich regions, particularly sub-cutaneous structures associated with injury or inflammation, to NGF-poor structures such as muscle or bone. Using immunohistological methods with primary antibodies to rhNGF, we report that NGF levels were elevated in 13 painful neuromas in comparison with six control nerves. However, in four painful neuromata re-located into muscle with pain relief, the NGF level was similar to that of controls. NGF levels suggest an explanation for the development of painful neuromas and the efficacy of relocation.

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