Cell stretching is amplified by active actin remodelling to deform and recruit proteins in mechanosensitive structures

AbstractMechanical stimulation of single cells has been shown to affect cellular behavior from the molecular scale to ultimate cell fate including apoptosis and proliferation. In this, the ability to control the spatiotemporal application of force on cells through their extracellular matrix connections is critical to understand the cellular response of mechanotransduction. Here, we develop and utilize a novel pressure-driven equibiaxial cell stretching device (PECS) combined with an elastomeric material to control specifically the mechanical stimulation on single cells. Cells were cultured on silicone membranes coated with molecular matrices and then a uniform pressure was introduced to the opposite surface of the membrane to stretch single cells equibiaxially. This allowed us to apply mechanical deformation to investigate the complex nature of cell shape and structure. These results will enhance our knowledge of cellular and molecular function as well as provide insights into fields including biomechanics, tissue engineering, and drug discovery.

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Single-Cell Stretching in Viscoelastic Fluids with Electronically Triggered Imaging for Cellular Mechanical Phenotyping

Analytical Chemistry ◽

10.1021/acs.analchem.0c05009 ◽

2021 ◽

Author(s):

Minhui Liang ◽

Dahou Yang ◽

Yinning Zhou ◽

Peixian Li ◽

Jianwei Zhong ◽

...

Keyword(s):

Single Cell ◽

Viscoelastic Fluids ◽

Cell Stretching

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Rab13 regulates PKA signaling during tight junction assembly

The Journal of Cell Biology ◽

10.1083/jcb.200312118 ◽

2004 ◽

Vol 165 (2) ◽

pp. 175-180 ◽

Cited By ~ 69

Author(s):

Katja Köhler ◽

Daniel Louvard ◽

Ahmed Zahraoui

Keyword(s):

Tight Junction ◽

Tight Junctions ◽

Inhibitory Effect ◽

Cell Junctions ◽

Unknown Mechanism ◽

Epithelial Tight Junctions ◽

Actin Remodelling ◽

Cell Cell

The GTPase Rab13 regulates the assembly of functional epithelial tight junctions (TJs) through a yet unknown mechanism. Here, we show that expression of the GTP-bound form of Rab13 inhibits PKA-dependent phosphorylation and TJ recruitment of the vasodilator-stimulated phosphoprotein, an actin remodelling protein. We demonstrate that Rab13GTP directly binds to PKA and inhibits its activity. Interestingly, activation of PKA abrogates the inhibitory effect of Rab13 on the recruitment of vasodilator-stimulated phosphoprotein, ZO-1, and claudin1 to cell–cell junctions. Rab13 is, therefore, the first GTPase that controls PKA activity and provides an unexpected link between PKA signaling and the dynamics of TJ assembly.

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Real-Time Measurement of F-Actin Remodelling during Exocytosis Using Lifeact-EGFP Transgenic Animals

PLoS ONE ◽

10.1371/journal.pone.0039815 ◽

2012 ◽

Vol 7 (7) ◽

pp. e39815 ◽

Cited By ~ 19

Author(s):

Yujin Jang ◽

Carolina Soekmadji ◽

Justin M. Mitchell ◽

Walter G. Thomas ◽

Peter Thorn

Keyword(s):

Real Time ◽

Transgenic Animals ◽

Time Measurement ◽

Real Time Measurement ◽

Actin Remodelling

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The Role of p38 MAPK and Its Substrates in Neuronal Plasticity and Neurodegenerative Disease

Journal of Signal Transduction ◽

10.1155/2012/649079 ◽

2012 ◽

Vol 2012 ◽

pp. 1-12 ◽

Cited By ~ 107

Author(s):

Sônia A. L. Corrêa ◽

Katherine L. Eales

Keyword(s):

Neurodegenerative Diseases ◽

P38 Mapk ◽

Mitogen Activated Protein Kinase ◽

Cellular Mechanisms ◽

Cellular Localisation ◽

Mapk Signalling ◽

Mitogen Activated Protein ◽

Normal Ageing ◽

Actin Remodelling

A significant amount of evidence suggests that the p38-mitogen-activated protein kinase (MAPK) signalling cascade plays a crucial role in synaptic plasticity and in neurodegenerative diseases. In this review we will discuss the cellular localisation and activation of p38 MAPK and the recent advances on the molecular and cellular mechanisms of its substrates: MAPKAPK 2 (MK2) and tau protein. In particular we will focus our attention on the understanding of the p38 MAPK-MK2 and p38 MAPK-tau activation axis in controlling neuroinflammation, actin remodelling and tau hyperphosphorylation, processes that are thought to be involved in normal ageing as well as in neurodegenerative diseases. We will also give some insight into how elucidating the precise role of p38 MAPK-MK2 and p38 MAPK-tau signalling cascades may help to identify novel therapeutic targets to slow down the symptoms observed in neurodegenerative diseases such as Alzheimer's and Parkinson's disease.

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