Down-regulation of ERK but not MEK phosphorylation in cultured endothelial cells by repeated changes in cyclic stretch

Shi, Feng; Chiu, Yi Jen; Cho, Youngsun; Bullard, Tara A.; Sokabe, Masahiro; Fujiwara, Keigi

doi:10.1016/j.cardiores.2006.12.014

Cited by 19 publications

(12 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At each increment in strain amplitude, stretching-induced signaling should re-occur 33 ; therefore, the culture medium was changed prior to each incrementation step with a fresh 5 M dose of SB203580. After an eight step incrementation regime from 2.5–9.5% strain amplitude over three weeks, the final collagen content of the tissue constructs was determined.…”

Section: Resultsmentioning

confidence: 99%

Combating Adaptation to Cyclic Stretching by Prolonging Activation of Extracellular Signal-Regulated Kinase

2013

View full text Add to dashboard Cite

In developing implantable tissues based on cellular remodeling of a fibrin scaffold, a key indicator of success is high collagen content. Cellular collagen synthesis is stimulated by cyclic stretching but is limited by cellular adaptation. Adaptation is mediated by deactivation of extracellular signal-regulated kinase (ERK); therefore inhibition of ERK deactivation should improve mechanically stimulated collagen production and accelerate the development of strong engineered tissues. The hypothesis of this study is that p38 mitogen activated protein kinase (p38) activation by stretching limits ERK activation and that chemical inhibition of p38/isoforms with SB203580 will increase stretching-induced ERK activation and collagen production. Both p38 and ERK were activated by 15 minutes of stretching but only p38 remained active after 1 hour. After an effective dose of inhibitor was identified using cell monolayers, 5 M SB203580 was found to increase ERK activation by two-fold in cyclically stretched fibrin-based tissue constructs. When 5 M SB203580 was added to the culture medium of constructs exposed to three weeks of incremental amplitude cyclic stretch, 2.6 fold higher stretching-induced total collagen was obtained. In conclusion, SB203580 circumvents adaptation to stretching induced collagen production and may be useful in engineering tissues where mechanical strength is a priority.

show abstract

Section: Resultsmentioning

confidence: 99%

Combating Adaptation to Cyclic Stretching by Prolonging Activation of Extracellular Signal-Regulated Kinase

2013

View full text Add to dashboard Cite

show abstract

“…Cyclic strains modulate the endothelial ECM composition and matrix metalloproteinase (MMP) expression; see (Cummins et al, 2007) for a review. Interestingly, some of the signaling mechanisms by which ECs sense shear stress have also been implicated in the sensing of stretch (Shi et al, 2007). There are a number of excellent reviews which address these and other strain-initiated signaling responses (Kakisis et al, 2004;Pradhan and Sumpio, 2004;Cummins et al, 2007).…”

Section: Cyclic Strainmentioning

confidence: 99%

Exogenous and endogenous force regulation of endothelial cell behavior

Califano

Reinhart‐King

2010

Journal of Biomechanics

111

View full text Add to dashboard Cite

“…Postphosphorylation PECAM-1 binds to SHP-2 (57), a protein tyrosine phosphatase involved in ERK1/2 activation. Because ERK1/2 is activated by flow (85) and stretch (81) in ECs, this activation may depend on PECAM-1 phosphorylation and subsequent binding to SHP-2 (67). SHP-2 is a cytoplasmic protein, but shortly after ECs are challenged with mechanical stresses, SHP-2 is recruited to the cell-cell contact region where PECAM-1 is localized (67).…”

Section: Mechanism Of Pecam-1 Mechanotransduction In Endothelial Cellmentioning

confidence: 99%

Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses

Chatterjee

Fujiwara

Pérez

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

Chatterjee S, Fujiwara K, Pérez NG, Ushio-Fukai M, Fisher AB. Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses. Am J Physiol Heart Circ Physiol 308: H1451-H1462, 2015. First published April 10, 2015; doi:10.1152/ajpheart.00105.2015.-Cells are constantly exposed to mechanical forces that play a role in modulating cellular structure and function. The cardiovascular system experiences physical forces in the form of shear stress and stretch associated with blood flow and contraction, respectively. These forces are sensed by endothelial cells and cardiomyocytes and lead to responses that control vascular and cardiac homeostasis. This was highlighted at the Pan American Physiological Society meeting at Iguassu Falls, Brazil, in a symposium titled "Mechanosignaling in the Vasculature." This symposium presented recent research that showed the existence of a vital link between mechanosensing and downstream redox sensitive signaling cascades. This link helps to transduce and transmit the physical force into an observable physiological response. The speakers showcased how mechanosensors such as ion channels, membrane receptor kinases, adhesion molecules, and other cellular components transduce the force via redox signals (such as reactive oxygen species and nitric oxide) to receptors (transcription factors, growth factors, etc.). Receptor activated pathways then lead to cellular responses including cellular proliferation, contraction, and remodeling. These responses have major relevance to the physiology and pathophysiology of various cardiovascular diseases. Thus an understanding of the complex series of events, from the initial sensing through the final response, is essential for progress in this field. Overall, this symposium addressed some important emerging concepts in the field of mechanosignaling and the eventual pathophysiological responses. Anrep effect; mechanotransduction; NADPH oxidase; revascularization; vasculature THIS ARTICLE is part of a collection on 1st PanAmerican Congress of Physiological Sciences: Physiology Without Borders. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http:// ajpheart.physiology.org/.Cells in vivo are constantly exposed to the physical forces associated with their local environment. Although it was well known that forces such as gravity and friction act on organisms and affect their function and structure, it is only in the last two decades that the complex processes by which these forces are sensed by cells is becoming clear (37,48,55,98). Cells and indeed cellular structures respond to external forces in a manner similar to chemical signaling where chemicals (ligands) bind to specific receptors on cells and initiate cellular signaling and an eventual response (24,26,36). Likewise, mechanical signaling or mechanotransduction involves the activation of receptors. Analogous to chemical signaling or chemotransduction, physical forces trigger a signaling proces...

show abstract

Down-regulation of ERK but not MEK phosphorylation in cultured endothelial cells by repeated changes in cyclic stretch

Cited by 19 publications

References 53 publications

Combating Adaptation to Cyclic Stretching by Prolonging Activation of Extracellular Signal-Regulated Kinase

Combating Adaptation to Cyclic Stretching by Prolonging Activation of Extracellular Signal-Regulated Kinase

Exogenous and endogenous force regulation of endothelial cell behavior

Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses

Contact Info

Product

Resources

About