Mechanical stimulation prevents osteocyte apoptosis: Requirement of integrins, Src kinases, and ERKs

Lilian Plotkin, I. Mathov, J. I. Aguirre, A. M. Parfitt, S. C. Manolagas, Teresita Bellido

Research output: Contribution to journalArticle

173 Citations (Scopus)

Abstract

Osteocytes, former osteoblasts entombed in the bone matrix, form an extensive cell communication network that is thought to detect microdamage and mechanical strains and to transmit signals leading to repair and compensatory bone augmentation or reduction. Bone active hormones and drugs control the integrity of this network by regulating osteocyte apoptosis, which might be a determinant of bone strength. Herein we demonstrate that mechanical stimulation by stretching activates the ERKs, which in turn are responsible for the attenuation of osteocyte apoptosis. The effect of osteocyte stretching is transmitted by integrins and cytoskeletal and catalytic molecules, such as Src kinases. Stretch-induced antiapoptosis also requires nuclear translocation of ERKs and new gene transcription. The evidence linking mechanical stimulation, activation of an integrin/cytoskeleton/Src/ERK signaling pathway, and osteocyte survival provides a mechanistic basis for the profound role of mechanical forces, or lack thereof, on skeletal health and disease.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume289
Issue number3 58-3
DOIs
StatePublished - Sep 2005
Externally publishedYes

Fingerprint

Osteocytes
src-Family Kinases
Integrins
Bone
Apoptosis
Stretching
Bone and Bones
Osteoblasts
Transcription
Bone Matrix
MAP Kinase Signaling System
Drug and Narcotic Control
Telecommunication networks
Cytoskeleton
Repair
Cell Communication
Genes
Chemical activation
Health
Hormones

Keywords

  • Bone
  • Caveolae
  • Mechanotransduction
  • Osteoblastic cells
  • Stretching

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

Mechanical stimulation prevents osteocyte apoptosis : Requirement of integrins, Src kinases, and ERKs. / Plotkin, Lilian; Mathov, I.; Aguirre, J. I.; Parfitt, A. M.; Manolagas, S. C.; Bellido, Teresita.

In: American Journal of Physiology - Cell Physiology, Vol. 289, No. 3 58-3, 09.2005.

Research output: Contribution to journalArticle

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