Molecular regulation of mechanotransduction

Biochem Biophys Res Commun. 2005 Mar 18;328(3):751-5. doi: 10.1016/j.bbrc.2004.12.087.

Abstract

There is a common mechanism for mechanotransduction in cells, regardless of the cell type. Integrins, interacting with their matrix/environment, mediate increases in intracellular Ca2+ levels and activate MAP kinase cascades to cause ERK1/2 phosphorylation. Phosphorylated ERK1/2 causes the activation of the AP-1 family of transcription factors that are necessary for the pro-growth response. The pro-bone growth response involves upregulation of the genes c-fos, IGF-1, cyclooxygenase, and osteocalcin. In osteocytes, increases in intracellular Ca2+ levels may additionally occur by extracellular Ca2+ influx through a stretch-activated ion channel. Each bone cell appears fine-tuned for the type of stimulus, with accessory mechanotransduction signaling pathways, such as calcineurin-mediated activation of the tissue-specific transcription factor NF-AT, adjusting the outcome of signaling in each case.

Publication types

  • Review

MeSH terms

  • Animals
  • Bone Development / physiology*
  • Bone Matrix / physiology*
  • Calcium Signaling / physiology*
  • Cytokines / physiology*
  • Extracellular Matrix / physiology
  • Humans
  • Integrins / metabolism*
  • Mechanotransduction, Cellular / physiology*
  • Osteocytes / physiology*

Substances

  • Cytokines
  • Integrins