Noda Mechanosensing Biology

1. Auflage 2010
ISBN: 978-4-431-89757-6
Verlag: Springer Japan
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 219 Seiten

Mechanical stress is vital to the functioning of the body, especially for tissues such as bone, muscle, heart, and vessels. It is well known that astronauts and bedridden patients suffer muscle and bone loss from lack of use. Even the heart, in pumping blood, causes mechanical stress to itself and to vascular tissue. With the loss of mechanical stress, homeostasis becomes impaired and leads to pathological conditions such as osteopenia, muscle atrophy, and vascular tissue dysfunction. In elderly populations, such mechanical pathophysiology, as well as the mechanical activities of locomotor and cardiovascular systems, is important because skeletal and heart functions decline and cause diseases in other organs. In this monograph, mechanical stress is discussed by experts in the field with respect to molecular, cellular, and tissue aspects in relation to medicine. Covering topics such as gravity and tissues and disuse osteoporosis, the book provides the most up-to-date information on cutting-edge advancements in the field of mechanobiology and is a timely contribution to research into locomotor and circulatory diseases that are major problems in contemporary society.

Autoren/Hrsg.

Noda, Masaki

Inhaltsverzeichnis

1;Noda_FM_O.pdf;1
2;Noda_Ch01_O.pdf;15
2.1;Chapter 1: Nanotechnology in Mechanobiology: Mechanical Manipulation of Cells and Organelle While Monitoring Intracellular S;16
2.1.1;1.1 Introduction;16
2.1.2;1.2 A Variety of Methods for Applying Forces to Cells and Analyses of Mechanosensing and Signaling;17
2.1.2.1;1.2.1 Stretching Cells Cultured on Elastic Sheets;17
2.1.2.2;1.2.2 Localized Force Application by Dragging a Pipette While Recording Intracellular Signaling;18
2.1.2.3;1.2.3 Mechanical Force Application to the Cell Surface by Optically Dragging a Bead for Analyzing the Contact Formation;20
2.1.2.4;1.2.4 Force Application Via a Bead Attached on the Surface of a Cell for the Analyses with High Spatial–Temporal Resolution;21
2.1.2.5;1.2.5 Mechanical Stretching of Actin Stress Fibers by Displacing a FN-Bead to Activate MS Channels in HUVECs;23
2.1.2.6;1.2.6 Direct Mechanical Stretching of Actin Stress Fibers by Dragging Beads Optically to Activate MS Channels;26
2.1.2.7;1.2.7 [Ca2+]i Microdomains in the Vicinity of the FCs Apparently Correspond to the MS Ca2+ Permeable Channels;27
2.1.3;1.3 Roles of Mechanosensing in Cell Migration;29
2.1.4;1.4 Future Perspectives;30
2.1.5;References;30
3;Noda_Ch02_O.pdf;33
3.1;Chapter 2: Molecular Mechanisms Underlying Mechanosensing in Vascular Biology;33
3.1.1;2.1 Introduction;33
3.1.2;2.2 EC Responses to Shear Stress;34
3.1.3;2.3 Shear Stress Mechanotransduction;35
3.1.3.1;2.3.1 Shear Stress Signaling Pathways;35
3.1.3.2;2.3.2 Shear Stress Sensors;35
3.1.3.2.1;2.3.2.1 Ion Channels;36
3.1.3.2.1.1;P2X4 Channel-Mediated Ca2+ Signaling of Shear Stress;37
3.1.3.2.1.2;Roles of Shear Stress Ca2+ Signaling in Control of Circulatory System;39
3.1.3.2.2;2.3.2.2 Tyrosine Kinase Receptors;39
3.1.3.2.3;2.3.2.3 G Proteins;40
3.1.3.2.4;2.3.2.4 Caveolae;40
3.1.3.2.5;2.3.2.5 Adhesion Proteins;41
3.1.3.2.6;2.3.2.6 Cytoskeleton;42
3.1.3.2.7;2.3.2.7 Glycocalyx;42
3.1.3.2.8;2.3.2.8 Primary Cilia;43
3.1.4;2.4 Conclusion;43
3.1.5;References;44
4;Noda_Ch03_O.pdf;50
4.1;Chapter 3: Mechanobiology During Vertebrate Organ Development;50
4.1.1;3.1 Regulation of Neural Crest Cell Migration;50
4.1.2;3.2 Integration of Mechanical Information by Neuronal Cells In Vitro;51
4.1.3;3.3 Differentiation of Pronephros;54
4.1.4;3.4 Effect of Gravity and Shear Stress on Dome Structure Formation in a Tubulogenesis Model;55
4.1.5;References;56
5;Noda_Ch04_O.pdf;59
5.1;Chapter 4: Mechanobiology in Skeletal Muscle: Conversion of Mechanical Information into Molecular Signal;60
5.1.1;4.1 Introduction;60
5.1.2;4.2 Mechanosensor in Skeletal Muscle;61
5.1.2.1;4.2.1 Experimental Models for Mechanotransduction;61
5.1.2.2;4.2.2 Mechanosensors in Skeletal Muscle;62
5.1.2.3;4.2.3 Stretch-Activated Channels;62
5.1.2.4;4.2.4 Neuronal Nitric Oxide Synthase and Mechanotransduction;63
5.1.2.5;4.2.5 nNOS and Unloading;64
5.1.2.6;4.2.6 Phospholipase D and Phosphatidic Acid;65
5.1.2.7;4.2.7 Integrins/FAK Signaling and Mechanotransduction;65
5.1.2.8;4.2.8 Sarcomere and Mechanotransduction;66
5.1.2.9;4.2.9 Growth Factors and Overload;66
5.1.3;4.3 Signaling Pathways in Mechanotransduction;66
5.1.3.1;4.3.1 mTOR Is a Key Signaling Molecule for Mechanical Overload-Induced Muscle Hypertrophy;67
5.1.3.2;4.3.2 Unload (Inactivity or Disuse) and the Catabolic Signaling Pathway;67
5.1.3.2.1;4.3.2.1 Downstream Targets of NF-kB and FoxO Transcription Factors;68
5.1.4;4.4 Conclusion;68
5.1.5;References;68
6;Noda_Ch05_O.pdf;72
6.1;Chapter 5: Mechanobiology in Space;72
6.1.1;5.1 Introduction;72
6.1.2;5.2 Unloading and Protein Degradation;73
6.1.3;5.3 Muscle Specific Ubiquitin Ligases;74
6.1.4;5.4 Deactivation of IGF-1/PI3K/Akt Pathway;76
6.1.5;5.5 Myostatin;76
6.1.6;5.6 Summary and Perspective;77
6.1.7;References;77
7;Noda_Ch06_O.pdf;80
7.1;Chapter 6: Mechanical Stress and Bone;80
7.1.1;6.1 Introduction;80
7.1.2;6.2 Nervous System Is Involved in Unloading-Induced Bone Loss;81
7.1.3;6.3 Central Control of Bone Mass Under Unloading Condition;83
7.1.4;6.4 Calcium Channel Involvement in Unloading-Induced Bone Loss;84
7.1.5;6.5 Tooth Movement Model and Extracellular Matrix Protein Action in Mechanical Stimulation;85
7.1.6;6.6 Transcription Factor Modulates Unloading-Induced Bone Loss;86
7.1.7;6.7 Unloading-Induced Bone Loss Requires Nucleocytoplasmic Shuttling Protein;87
7.1.8;6.8 Interaction of PTH Signaling and Unloading;89
7.1.9;6.9 Role of Noncollagenous Matrix Protein, OPN, in Bone in Unloading-Induced Bone Loss;91
7.1.10;6.10 Role of Noncollagenous Matrix Protein, OPN in Mechanical Force Dependent Bone Formation;91
7.1.11;6.11 Intracellular Mechanism of Sensing Mechanical Stress;92
7.1.12;6.12 Conclusion;93
7.1.13;References;93
8;Noda_Ch07_O.pdf;96
8.1;Chapter 7: TRP Channels and Mechanical Signals;96
8.1.1;7.1 Transient Receptor Potential Channels;96
8.1.2;7.2 TRPC Channels: Activation by Direct Stretch Via a Lipid-Dependent Mechanism;98
8.1.3;7.3 TRPM Channel: Is It Mechanosensitive?;100
8.1.4;7.4 TRPA1: Activation by Interaction of Cell Cytoskeleton?;101
8.1.5;7.5 TRPV: Activation by Mechanical Stress Through Lipid Metabolites;101
8.1.6;7.6 TRPP2: Making a Flow-Sensing Complex with TRPV4;105
8.1.7;7.7 Hypothesis: Mechanosensitive Channel Complex;106
8.1.8;References;107
9;Noda_Ch08_O.pdf;111
9.1;Chapter 8: Osteoblast Biology and Mechanosensing;112
9.1.1;8.1 Mechanical Forces and Skeletal Integrity;112
9.1.2;8.2 Effects of Mechanical Forces on Osteoblastogenesis;113
9.1.2.1;8.2.1 Osteoblast Biology;113
9.1.2.2;8.2.2 Osteoblast Responses to Mechanical Forces;113
9.1.2.3;8.2.3 Effects of Mechanical Forces on Osteoblastogenesis In Vivo;114
9.1.3;8.3 Mechanosensing Mechanisms in Osteoblasts;117
9.1.3.1;8.3.1 Mechanical Stimuli;117
9.1.3.2;8.3.2 Mechanoreceptors;117
9.1.4;8.4 Role of Wnt Signaling in Mechanotransduction in Osteoblasts;120
9.1.5;8.5 Mechanoresponsive Genes in Osteoblasts;120
9.1.5.1;8.5.1 Transcription Factors;120
9.1.5.2;8.5.2 Soluble Mediators;121
9.1.5.3;8.5.3 Growth Factors;123
9.1.5.4;8.5.4 Matrix Proteins;124
9.1.6;8.6 Conclusions;124
9.1.7;References;125
10;Noda_Ch09_O.pdf;134
10.1;Chapter 9: Osteocytes in Mechanosensing: Insights from Mouse Models and Human Patients;134
10.1.1;9.1 Introduction;134
10.1.2;9.2 Osteocytes in Aging and Disease;134
10.1.3;9.3 Osteocytes in Genetically Modified Mice;136
10.1.4;9.4 Insights from a Mouse Model Lacking Osteocytes;137
10.1.5;9.5 Osteocyte-Derived Factors that Regulate Bone Metabolism;138
10.1.6;9.6 Conclusion;142
10.1.7;References;142
11;Noda_Ch10_O.pdf;147
11.1;Chapter 10: Osteocyte Mechanosensation and Transduction;147
11.1.1;10.1 Introduction;147
11.1.2;10.2 The Osteocyte as a Mechanosensory Cell;148
11.1.3;10.3 In Vitro Cell Culture Models;149
11.1.4;10.4 Cell Body, Cell Process, Cilia;151
11.1.5;10.5 Signaling Pathways Used by Osteocytes in Response to Loading;152
11.1.6;10.6 Role of Integrins in Osteocyte Mechanotransduction;154
11.1.7;10.7 Influence of the Osteocyte Perilacunar Matrix on Mechanosensation;156
11.1.8;10.8 Looking to the Future;157
11.1.9;References;158
12;Noda_Ch11_O.pdf;162
12.1;Chapter 11: Mechanosensing and Signaling Crosstalks;162
12.1.1;11.1 Introduction;163
12.1.2;11.2 Mechanosensors and Signaling Systems;163
12.1.3;11.3 Fos Family Gene Expression in Response to Mechanical Stress;164
12.1.4;11.4 Enhanced IL-11 Expression by Mechanical Stress;166
12.1.5;11.5 Mechanical Stress Upregulates IL-11 Via DFosB/JunD Binding to the AP-1 Site;166
12.1.6;11.6 Smad Signaling in Response to Mechanical Stress;167
12.1.7;11.7 AP-1 and Smad Signaling Pathways Merge on IL-11 Gene Promoter;168
12.1.8;11.8 Stimulation of Canonical Wnt Signaling Downstream IL-11;168
12.1.9;References;169
13;Noda_Ch12_O.pdf;172
13.1;Chapter 12: Osteoblast Development in Bone Loss Due to Skeletal Unloading;172
13.1.1;12.1 Introduction;172
13.1.2;12.2 Materials and Methods;173
13.1.2.1;12.2.1 Experimental Design;173
13.1.2.2;12.2.2 Histomorphometry;173
13.1.2.3;12.2.3 Flow Cytometry;173
13.1.2.4;12.2.4 Cell Culture;174
13.1.2.5;12.2.5 ALP Production of Cultured Cells;174
13.1.2.6;12.2.6 Quantitative Real-Time Reverse-Transcriptase-Polymerase Chain Reactions;174
13.1.2.7;12.2.7 Statistical Analysis;175
13.1.3;12.3 Results;175
13.1.3.1;12.3.1 Bone Volume After Unloading and Reloading;175
13.1.3.2;12.3.2 Bone Volume and Formation in Disrupted p53 Gene;175
13.1.3.3;12.3.3 PECAM-1 Expression After Unloading;177
13.1.3.4;12.3.4 Bone Marrow Cell Development;177
13.1.4;12.4 Discussion;178
13.1.5;References;182
14;Noda_Ch13_O.pdf;184
14.1;Chapter 13: Mechanosensing in Bone and the Role of Glutamate Signalling;185
14.1.1;13.1 Introduction;185
14.1.2;13.2 Modes of Loading Affecting the Skeleton;186
14.1.3;13.3 Components of Osteogenic Strains: Strain Magnitude;187
14.1.4;13.4 Strain Rate and Frequency;188
14.1.5;13.5 Strain Direction;189
14.1.6;13.6 Strain Regimen Duration, Repetition and Interruption;190
14.1.7;13.7 Site Specificity of Habitual Bone Strains;190
14.1.8;13.8 Inferences from the Known Effects of Altered Loading;191
14.1.9;13.9 The Role of Glutamate Signalling in the Skeleton’s “Strain Memory”;192
14.1.10;13.10 Conclusions;193
14.1.11;References;193
15;Noda_Ch14_O.pdf;196
15.1;Chapter 14: Osteoclast Biology and Mechanosensing;196
15.1.1;14.1 Introduction;196
15.1.2;14.2 Podosomes: Recently Proven Mechanosensors;199
15.1.3;14.3 Importance of Mechanical Signals During Osteoclast Differentiation;200
15.1.3.1;14.3.1 Osteoclast Differentiation: The Bone Touch;200
15.1.3.2;14.3.2 The Need for an Appropriate Experimental System;201
15.1.3.3;14.3.3 Osteoclast Differentiation Requires a Stiff Substrate;201
15.1.3.4;14.3.4 Strain Inhibits Osteoclast Differentiation;203
15.1.3.5;14.3.5 Microgravity Stimulates Osteoclast Differentiation;204
15.1.4;14.4 Importance of Mechanical Signals for Bone Resorption by Osteoclasts;205
15.1.4.1;14.4.1 Mature Osteoclasts Sense and Respond to Matrix Stiffness;205
15.1.4.2;14.4.2 Bone Resorption: The Influence of Mechanical Stimulation;206
15.1.4.3;14.4.3 Can Osteoclasts Recognize and Adapt to Topographical Features?;207
15.1.5;14.5 Molecular Pathways Involved in Osteoclast Response to Mechanical Stimuli;209
15.1.5.1;14.5.1 Transduction of Mechanical Signal Through Integrin a.vb.3, p130Cas and Src Family Tyrosine Kinases in Osteoclasts?;209
15.1.5.2;14.5.2 Effectors of Mechanical Signals in Osteoclasts: Myosin IIA and Rho Family GTPases;210
15.1.6;14.6 Conclusion;211
15.1.7;References;212
16;Noda_Index_O.pdf;217
16.1;b978-0-387-78701_4;217