Cellular and Molecular Mechanotransduction in Bone

Julia C. Chen, Alesha Castillo, Christopher R. Jacobs

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

This chapter reviews the state of knowledge with respect to skeletal mechanobiology. Forms of tissue-level mechanical stimulation are first described, including electromagnetic fields, strain, fluid flow, vibration, and damage. The resulting biophysical environment at the cellular and pericellular level is also considered. However, for a biological response to occur in response to loading, mechanical signals must induce cellular biochemical signaling. How bone and progenitor cells may sense their mechanical environment is addressed by describing potential candidates for molecular transduction of mechanical to biochemical signaling. Candidates include cytoskeletal proteins, integrins and adhesion-associated proteins, membrane channels, plasma membrane dynamics, mechanosomes, and primary cilia. Furthermore, mechanically activated intracellular signaling pathways involving calcium, G-proteins, and kinases, as well as cell-cell pathways involving gap junctions, nitric oxide, eicosanoids, stromal cell-derived factor-1, and nucleotides are discussed. Progress toward understanding mechanisms involved in bone mechanotransduction holds great potential in providing therapeutic targets to the disease of osteoporosis.

Original languageEnglish (US)
Title of host publicationOsteoporosis: Fourth Edition
PublisherElsevier Inc.
Pages453-475
Number of pages23
ISBN (Print)9780124158535
DOIs
StatePublished - Jun 2013

Fingerprint

Cellular Mechanotransduction
Biophysics
Chemokine CXCL12
Bone and Bones
Cyclic GMP-Dependent Protein Kinases
Gastrin-Secreting Cells
Electromagnetic Fields
Cytoskeletal Proteins
Eicosanoids
Cilia
Gap Junctions
Vibration
Ion Channels
GTP-Binding Proteins
Integrins
Osteoporosis
Nitric Oxide
Stem Cells
Nucleotides
Cell Membrane

Keywords

  • Annexin V
  • Bone
  • Bone matrix
  • Cytoskeleton
  • Eicosanoids
  • Electromagnetic fields
  • FAK
  • Fluid flow
  • Gap junctions
  • GPCRs
  • Integrins
  • Intracellular calcium signaling
  • Mechanosensors
  • Mechanostat theory
  • Mechanotransduction
  • NO signaling
  • Nucleotide
  • Osteocytes
  • Pericellular flow
  • Pressure
  • Primary cilia
  • Skeletal mechanobiology
  • Tissue mechanics

ASJC Scopus subject areas

  • Medicine(all)
  • Dentistry(all)

Cite this

Chen, J. C., Castillo, A., & Jacobs, C. R. (2013). Cellular and Molecular Mechanotransduction in Bone. In Osteoporosis: Fourth Edition (pp. 453-475). Elsevier Inc.. https://doi.org/10.1016/B978-0-12-415853-5.00020-0

Cellular and Molecular Mechanotransduction in Bone. / Chen, Julia C.; Castillo, Alesha; Jacobs, Christopher R.

Osteoporosis: Fourth Edition. Elsevier Inc., 2013. p. 453-475.

Research output: Chapter in Book/Report/Conference proceedingChapter

Chen, JC, Castillo, A & Jacobs, CR 2013, Cellular and Molecular Mechanotransduction in Bone. in Osteoporosis: Fourth Edition. Elsevier Inc., pp. 453-475. https://doi.org/10.1016/B978-0-12-415853-5.00020-0
Chen JC, Castillo A, Jacobs CR. Cellular and Molecular Mechanotransduction in Bone. In Osteoporosis: Fourth Edition. Elsevier Inc. 2013. p. 453-475 https://doi.org/10.1016/B978-0-12-415853-5.00020-0
Chen, Julia C. ; Castillo, Alesha ; Jacobs, Christopher R. / Cellular and Molecular Mechanotransduction in Bone. Osteoporosis: Fourth Edition. Elsevier Inc., 2013. pp. 453-475
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