Book contents
- Frontmatter
- Contents
- Contributors
- Preface
- 1 Introduction
- 2 Endothelial Mechanotransduction
- 3 Role of the Plasma Membrane in Endothelial Cell Mechanosensation of Shear Stress
- 4 Mechanotransduction by Membrane-Mediated Activation of G-Protein Coupled Receptors and G-Proteins
- 5 Cellular Mechanotransduction: Interactions with the Extracellular Matrix
- 6 Role of Ion Channels in Cellular Mechanotransduction – Lessons from the Vascular Endothelium
- 7 Toward a Modular Analysis of Cell Mechanosensing and Mechanotransduction
- 8 Tensegrity as a Mechanism for Integrating Molecular and Cellular Mechanotransduction Mechanisms
- 9 Nuclear Mechanics and Mechanotransduction
- 10 Microtubule Bending and Breaking in Cellular Mechanotransduction
- 11 A Molecular Perspective on Mechanotransduction in Focal Adhesions
- 12 Protein Conformational Change
- 13 Translating Mechanical Force into Discrete Biochemical Signal Changes
- 14 Mechanotransduction through Local Autocrine Signaling
- 15 The Interaction between Fluid-Wall Shear Stress and Solid Circumferential Strain Affects Endothelial Cell Mechanobiology
- 16 Micro- and Nanoscale Force Techniques for Mechanotransduction
- 17 Mechanical Regulation of Stem Cells
- 18 Mechanotransduction
- 19 Summary and Outlook
- Index
- Plate Section
19 - Summary and Outlook
Published online by Cambridge University Press: 05 July 2014
- Frontmatter
- Contents
- Contributors
- Preface
- 1 Introduction
- 2 Endothelial Mechanotransduction
- 3 Role of the Plasma Membrane in Endothelial Cell Mechanosensation of Shear Stress
- 4 Mechanotransduction by Membrane-Mediated Activation of G-Protein Coupled Receptors and G-Proteins
- 5 Cellular Mechanotransduction: Interactions with the Extracellular Matrix
- 6 Role of Ion Channels in Cellular Mechanotransduction – Lessons from the Vascular Endothelium
- 7 Toward a Modular Analysis of Cell Mechanosensing and Mechanotransduction
- 8 Tensegrity as a Mechanism for Integrating Molecular and Cellular Mechanotransduction Mechanisms
- 9 Nuclear Mechanics and Mechanotransduction
- 10 Microtubule Bending and Breaking in Cellular Mechanotransduction
- 11 A Molecular Perspective on Mechanotransduction in Focal Adhesions
- 12 Protein Conformational Change
- 13 Translating Mechanical Force into Discrete Biochemical Signal Changes
- 14 Mechanotransduction through Local Autocrine Signaling
- 15 The Interaction between Fluid-Wall Shear Stress and Solid Circumferential Strain Affects Endothelial Cell Mechanobiology
- 16 Micro- and Nanoscale Force Techniques for Mechanotransduction
- 17 Mechanical Regulation of Stem Cells
- 18 Mechanotransduction
- 19 Summary and Outlook
- Index
- Plate Section
Summary
Introduction
The primary objective of this book was to bring together various points of view on cellular mechanotransduction. This final, closing chapter attempts to summarize the various viewpoints discussed in previous chapters and establish a horizon for future research directions toward understanding the underlying processes involved in mechanotransduction.
Mechanotransduction is an essential function of the cell, controlling its growth, proliferation, protein synthesis, and gene expression. Extensive data exist documenting the cellular responses to external forces, but less is known about how force affects biological signaling. More generally, the question of how the mechanical and biochemical pathways interact remains largely unanswered. As articulated in the various chapters of this book, many studies during the past two decades have been carried out to shed light on a wide range of cellular responses to mechanical stimulation. It is well known that living cells can sense mechanical stimuli, and that forces applied to a cell or physical cues from the extracellular environment can elicit a wide range of biochemical responses that affect the cell’s phenotype in health and disease. It is now widely accepted that stresses experienced in vivo are instrumental in a wide spectrum of pathologies. One of the first diseases found to be linked to cellular stress was atherosclerosis, where it was demonstrated that hemodynamic shear influences endothelial function and that conditions of low or oscillatory shear stress are conducive to the formation and growth of atherosclerotic lesions. Similarly, the disease process of calcification in heart valves can be understood as a mechanotransduction phenomenon as valvular endothelial and interstitial cells tend to respond to pathophysiological stresses from disturbed blood flow patterns directly linked with abnormal deformations in the valve tissue. The role of mechanical stress on bone growth and healing was probably the first to be widely recognized, and since then many other stress-influenced cell functions have been identified.
- Type
- Chapter
- Information
- Cellular MechanotransductionDiverse Perspectives from Molecules to Tissues, pp. 438 - 444Publisher: Cambridge University PressPrint publication year: 2009