Mechanical stimulation of gap junctions in bone osteocytes is mediated by prostaglandin E2

Jean X. Jiang, Benxu Cheng

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Gap junction-mediated intercellular communications are thought to transduce the effects of mechanical strain from osteocytes to cells on the bone surface to initiate remodeling. To determine whether gap junctions may co-ordinate the effects of mechanical loading, osteocytelike MLO-Y4 cells were exposed to fluid flow-imposed shear stress. After exposure of MLOY4 to fluid flow, intercellular coupling increased in direct proportion to shear stress level. Interestingly, this stimulation is further enhanced during the post-stress period, indicating that released factor(s) is likely to be involved. The conditioned medium obtained from the fluid flow treated MLO-Y4 cells induced an increase in the number of functional gap junctions and Cx43 protein when added to non-sheer-stressed cells. Fluid flow was found to induce prostaglandin E2 (PGE2) release and increase cyclooxygenase 2 (COX-2) expression. When PGE2 was depleted from the fluid flow conditioned medium, the stimulatory effect on gap junctions was significantly decreased. Addition of the COX inhibitor indomethacin partially blocked the stimulatory effects of mechanical strain on gap junctions. Together, these studies suggest that the stimulatory effect of fluid flow on gap junctions is mediated in part by de novo synthesis and release of PGE2. Gap junctions may serve as channels for the signals generated by osteocytes in response to mechanical loading.

Original languageEnglish (US)
Pages (from-to)283-288
Number of pages6
JournalCell Adhesion and Communication
Issue number4-6
StatePublished - Dec 1 2000


  • Connexin 43
  • Fluid flow
  • Gap junctions
  • Osteocyte-like MLO-Y4 cells
  • PGE

ASJC Scopus subject areas

  • Cell Biology


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