scholarly journals Stress fiber growth and remodeling determines cellular morphomechanics under uniaxial cyclic stretch

2019 ◽  
Author(s):  
Aritra Chatterjee ◽  
Paturu Kondaiah ◽  
Namrata Gundiah
Keyword(s):  
Effective Elastic Modulus ◽  
Stress Fiber ◽  
Cyclic Stretch ◽  
Stress Fibers ◽  
Avoidance Reaction ◽  
Cortical Actin ◽  
Fiber Growth ◽  
Induced Stress ◽  
Reorientation Dynamics ◽  
And Migration

AbstractStress fibers in the cytoskeleton are essential in maintaining cellular shape, and influence their adhesion and migration. Cyclic uniaxial stretching results in cellular reorientation orthogonal to the applied stretch direction via a strain avoidance reaction; the mechanistic cues in cellular mechanosensitivity to this response are currently underexplored. We show stretch induced stress fiber lengthening, their realignment and increased cortical actin in fibroblasts stretched over varied amplitudes and durations. Higher amounts of actin and alignment of stress fibers were accompanied with an increase in the effective elastic modulus of cells. Microtubules did not contribute to the measured stiffness or reorientation response but were essential to the nuclear reorientation. We modeled stress fiber growth and reorientation dynamics using a nonlinear, orthotropic, fiber-reinforced continuum representation of the cell. The model predicts the observed fibroblast morphology and increased cellular stiffness under uniaxial cyclic stretch. These studies are important in exploring the differences underlying mechanotransduction and cellular contractility under stretch.

Mechanically Optimized Orientation of Intracellular Stress Fibers Under Cyclic Stretch

2000 ◽  
Author(s):  
Hiroshi Yamada ◽  
Tohru Takemasa ◽  
Takami Yamaguchi
Keyword(s):  
Endothelial Cell ◽  
Continuum Mechanics ◽  
Cellular Response ◽  
Length Change ◽  
Mechanical Stimulus ◽  
Stress Fiber ◽  
Cyclic Stretch ◽  
Stress Fibers ◽  
Biological Phenomenon ◽  
The Continuum

Abstract To elucidate the orientation of stress fibers in a cultured endothelial cell under cyclic stretch, we hypothesized that a stress fiber aligns so as to minimize the summation of its length change under cyclic stretch, and that there is a limit in the sensitivity of cellular response to the mechanical stimulus. Results from numerical simulations based on the continuum mechanics describe the experimental observations under uniaxial stretch well. They give us an insight to the biological phenomenon of the orientation in stress fibers under biaxial stretch from the viewpoint of mechanical engineering.

scholarly journals ADP-Ribosylation Factor 6 Regulates Actin Cytoskeleton Remodeling in Coordination with Rac1 and RhoA

2000 ◽  
Vol 20 (10) ◽  
pp. 3685-3694 ◽  
Author(s):  
Rita L. Boshans ◽  
Stacey Szanto ◽  
Linda van Aelst ◽  
Crislyn D'Souza-Schorey
Keyword(s):  
Cell Surface ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Dominant Negative ◽  
Stress Fibers ◽  
Cortical Actin ◽  
Adp Ribosylation ◽  
Stress Fiber Formation ◽  
Dependent Inhibition ◽  
Adp Ribosylation Factor

ABSTRACT In this study, we have documented an essential role for ADP-ribosylation factor 6 (ARF6) in cell surface remodeling in response to physiological stimulus and in the down regulation of stress fiber formation. We demonstrate that the G-protein-coupled receptor agonist bombesin triggers the redistribution of ARF6- and Rac1-containing endosomal vesicles to the cell surface. This membrane redistribution was accompanied by cortical actin rearrangements and was inhibited by dominant negative ARF6, implying that bombesin is a physiological trigger of ARF6 activation. Furthermore, these studies provide a new model for bombesin-induced Rac1 activation that involves ARF6-regulated endosomal recycling. The bombesin-elicited translocation of vesicular ARF6 was mimicked by activated Gαq and was partially inhibited by expression of RGS2, which down regulates Gq function. This suggests that Gq functions as an upstream regulator of ARF6 activation. The ARF6-induced peripheral cytoskeletal rearrangements were accompanied by a depletion of stress fibers. Moreover, cells expressing activated ARF6 resisted the formation of stress fibers induced by lysophosphatidic acid. We show that the ARF6-dependent inhibition of stress fiber formation was due to an inhibition of RhoA activation and was overcome by expression of a constitutively active RhoA mutant. The latter observations demonstrate that activation of ARF6 down regulates Rho signaling. Our findings underscore the potential roles of ARF6, Rac1, and RhoA in the coordinated regulation of cytoskeletal remodeling.

Analysis and Interpretation of Stress Fiber Organization in Cells Subject to Cyclic Stretch

2008 ◽  
Vol 130 (3) ◽  
Author(s):  
Zhensong Wei ◽  
Vikram S. Deshpande ◽  
Robert M. McMeeking ◽  
Anthony G. Evans
Keyword(s):  
Rate Sensitivity ◽  
Intrinsic Rate ◽  
Stress Fiber ◽  
Cyclic Stretch ◽  
Stress Fibers ◽  
Parameter Study ◽  
Cyclic Stretching ◽  
Cycling Frequency ◽  
Key Variables ◽  
Distribution Of Stress

Numerical simulations that incorporate a biochemomechanical model for the contractility of the cytoskeleton have been used to rationalize the following observations. Uniaxial cyclic stretching of cells causes stress fibers to align perpendicular to the stretch direction, with degree of alignment dependent on the stretch strain magnitude, as well as the frequency and the transverse contraction of the substrate. Conversely, equibiaxial cyclic stretching induces a uniform distribution of stress fiber orientations. Demonstrations that the model successfully predicts the alignments experimentally found are followed by a parameter study to investigate the influence of a range of key variables including the stretch magnitude, the intrinsic rate sensitivity of the stress fibers, the straining frequency, and the transverse contraction of the substrate. The primary predictions are as follows. The rate sensitivity has a strong influence on alignment, equivalent to that attained by a few percent of additional stretch. The fiber alignment increases with increasing cycling frequency. Transverse contraction of the substrate causes the stress fibers to organize into two symmetrical orientations with respect to the primary stretch direction.

scholarly journals Mechano-chemical control of human endothelium orientation and size.

1989 ◽  
Vol 109 (1) ◽  
pp. 331-339 ◽  
Author(s):  
V P Shirinsky ◽  
A S Antonov ◽  
K G Birukov ◽  
A V Sobolevsky ◽  
Y A Romanov ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Umbilical Vein ◽  
Giant Cells ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Cyclic Stretch ◽  
Stress Fibers ◽  
Conventional Culture ◽  
Orientation Response ◽  
Umbilical Vein Endothelial Cells

Human umbilical vein endothelial cells (EC) were grown on elastic silicone membranes subjected to cyclic stretch, simulating arterial wall motion. Stretching conditions (20% amplitude, 52 cycle/min) stimulated stress fiber formation and their orientation transversely to the strain direction. Cell bodies aligned along the same axis after the actin cytoskeleton. EC orientation response was inhibited by the adenylate cyclase activator, forskolin (10(-5) M), which caused stress fiber disassembly and the redistribution of F-actin to the cortical cytoplasm. Preoriented EC depleted of stress fibers by forskolin treatment retained their aligned state. Thus, stress fibers are essential for the process of EC orientation induced by repeated strain, but not for the maintenance of EC orientation. The monolayer formed by EC grown to confluence in conditions of intermittent strain consisted of uniform elongated cells and was resistant to deformation. In contrast, the monolayer assembled in stationary conditions was less compliant and exposed local denudations on initiation of stretching. When stretched in the presence of 10(-5) M forskolin it rapidly (3-4 h) reestablished integrity but gained a heterogeneous appearance since denuded areas were covered by giant cells. The protective effect of forskolin was because of the stimulation of EC spreading. This feature of forskolin was demonstrated while studying its action on EC spreading and repair of a scratched EC monolayer in conventional culture. Thus mechanical deformation and adenylate cyclase activity may be important factors in the control of endothelium morphology in human arteries.

scholarly journals Stretch-induced actin remodeling requires targeting of zyxin to stress fibers and recruitment of actin regulators

2012 ◽  
Vol 23 (10) ◽  
pp. 1846-1859 ◽  
Author(s):  
Laura M. Hoffman ◽  
Christopher C. Jensen ◽  
Aashi Chaturvedi ◽  
Masaaki Yoshigi ◽  
Mary C. Beckerle
Keyword(s):  
Mechanical Stimulation ◽  
Binding Capacity ◽  
Rho Kinase ◽  
Stress Fiber ◽  
Cyclic Stretch ◽  
Mitogen Activated Protein Kinase ◽  
Stress Fibers ◽  
Actin Remodeling ◽  
Mitogen Activated Protein ◽  
Actin Stress Fibers

Reinforcement of actin stress fibers in response to mechanical stimulation depends on a posttranslational mechanism that requires the LIM protein zyxin. The C-terminal LIM region of zyxin directs the force-sensitive accumulation of zyxin on actin stress fibers. The N-terminal region of zyxin promotes actin reinforcement even when Rho kinase is inhibited. The mechanosensitive integrin effector p130Cas binds zyxin but is not required for mitogen-activated protein kinase–dependent zyxin phosphorylation or stress fiber remodeling in cells exposed to uniaxial cyclic stretch. α-Actinin and Ena/VASP proteins bind to the stress fiber reinforcement domain of zyxin. Mutation of their docking sites reveals that zyxin is required for recruitment of both groups of proteins to regions of stress fiber remodeling. Zyxin-null cells reconstituted with zyxin variants that lack either α-actinin or Ena/VASP-binding capacity display compromised response to mechanical stimulation. Our findings define a bipartite mechanism for stretch-induced actin remodeling that involves mechanosensitive targeting of zyxin to actin stress fibers and localized recruitment of actin regulatory machinery.

scholarly journals Interplay between Solo and keratin filaments is crucial for mechanical force–induced stress fiber reinforcement

2016 ◽  
Vol 27 (6) ◽  
pp. 954-966 ◽  
Author(s):  
Sachiko Fujiwara ◽  
Kazumasa Ohashi ◽  
Toshiya Mashiko ◽  
Hiroshi Kondo ◽  
Kensaku Mizuno
Keyword(s):  
Tensile Force ◽  
Fiber Reinforcement ◽  
Stress Fiber ◽  
Mechanical Force ◽  
Fiber Formation ◽  
Stress Fibers ◽  
Nucleotide Exchange ◽  
Cellular Mechanisms ◽  
Rhoa Activation ◽  
Induced Stress

Mechanical force–induced cytoskeletal reorganization is essential for cell and tissue remodeling and homeostasis; however, the underlying cellular mechanisms remain elusive. Solo (ARHGEF40) is a RhoA-targeting guanine nucleotide exchange factor (GEF) involved in cyclical stretch–induced human endothelial cell reorientation and convergent extension cell movement in zebrafish gastrula. In this study, we show that Solo binds to keratin-8/keratin-18 (K8/K18) intermediate filaments through multiple sites. Solo overexpression promotes the formation of thick actin stress fibers and keratin bundles, whereas knockdown of Solo, expression of a GEF-inactive mutant of Solo, or inhibition of ROCK suppresses stress fiber formation and leads to disorganized keratin networks, indicating that the Solo-RhoA-ROCK pathway serves to precisely organize keratin networks, as well as to promote stress fibers. Of importance, knockdown of Solo or K18 or overexpression of GEF-inactive or deletion mutants of Solo suppresses tensile force–induced stress fiber reinforcement. Furthermore, knockdown of Solo or K18 suppresses tensile force-induced RhoA activation. These results strongly suggest that the interplay between Solo and K8/K18 filaments plays a crucial role in tensile force–induced RhoA activation and consequent actin cytoskeletal reinforcement.

The Direction of Cyclic Stretch-Induced Stress Fiber Orientation Depends on Matrix Rigidity

2011 ◽  
Author(s):  
Abhishek Tondon ◽  
Hui-Ju Hsu ◽  
Roland Kaunas
Keyword(s):  
Theoretical Model ◽  
Fiber Orientation ◽  
Stress Fiber ◽  
Cyclic Stretch ◽  
Matrix Rigidity ◽  
Structural Element ◽  
Cellular Processes ◽  
Induced Stress ◽  
Cellular Environment ◽  
Collagen Hydrogels

Mechanical properties of the cellular environment such as elastic rigidity have been shown to play an important role in the regulation of important cellular processes such as proliferation, differentiation and apoptosis (1–3). Intracellular tension decreases with decreasing matrix rigidity (1). Actin stress fibers (SFs), the major structural element in cells bearing tension, are also less prevalent on soft vs. rigid matrices (4). We have developed a theoretical model of stretch-induced SFs that predicts SFs reorient perpendicular to the direction of cyclic stretch in order to maintain SF tension at a homeostatic level (5). A theoretical model developed by the Safran group (6) predicts that cells will also align perpendicular to cyclic stretch on soft substrates. To test these predictions, we subjected cells to cyclic uniaxial stretch on soft collagen hydrogels. Interestingly, the cells and their SFs aligned parallel to the direction of stretch without co-alignment of collagen fibrils, indicating the need for a new model to describe the effects of cyclic stretch on SF reorganization on soft matrices.

Synergy between Rho signaling and matrix density in cyclic stretch-induced stress fiber organization

2014 ◽  
Vol 10 (5) ◽  
pp. 1876-1885 ◽  
Author(s):  
Jasper Foolen ◽  
Marloes W.J.T. Janssen-van den Broek ◽  
Frank P.T. Baaijens
Keyword(s):  
Stress Fiber ◽  
Cyclic Stretch ◽  
Matrix Density ◽  
Induced Stress ◽  
Fiber Organization

On the Intracellullar Memory of Stress Fiber Orientation: Effects of Microtubules and Focal Adhesions on the Repolymerization Process of Stress Fibers

2008 ◽  
Author(s):  
Yunfeng Yang ◽  
Kazuaki Nagayama ◽  
Takeo Matsumoto
Keyword(s):  
Fiber Orientation ◽  
Cell Movement ◽  
Focal Adhesions ◽  
Stress Fiber ◽  
Cyclic Stretch ◽  
Stress Fibers ◽  
Cellular Functions ◽  
Division 1 ◽  
Key Features ◽  
Strain Magnitude

Stress fibers (SFs) play essential roles in various cellular functions such as cell movement, shape maintenance and cell division [1]. One of their key features is that they dynamically change their structures in response to mechanical environment to which they are exposed [2]. For example, cultured endothelial cells exposed to cyclic stretch preferentially reorganize their actin stress fibers to the direction in which the strain magnitude of the fibers become minimum [3].

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