Fluid flow-induced prostaglandin E2 response of osteoblastic ROS 17/2.8 cells is gap junction-mediated and independent of cytosolic calcium

M. M. Saunders, J. You, Z. Zhou, Z. Li, Clare E Yellowley-genetos, E. L. Kunze, C. R. Jacobs, H. J. Donahue

Research output: Contribution to journalArticle

70 Citations (Scopus)

Abstract

It has been well demonstrated that bone adapts to mechanical loading. To accomplish this at the cellular level, bone cells must be responsive to mechanical loading (mechanoresponsive). This can occur via such mechanisms as direct cell deformation or signal transduction via complex pathways involving chemotransport, hormone response, and/or gene expression, to name a few. Mechanotransduction is the process by which a bone cell senses a biophysical signal and elicits a response. While it has been demonstrated that bone cells can respond to a wide variety of biophysical signals including fluid flow, stretch, and magnetic fields, the exact pathways and mechanisms involved are not clearly understood. We postulated that gap junctions may play an important role in bone cell responsiveness. Gap junctions (GJ) are membrane-spanning channels that physically link cells and support the transport of small molecules and ions in the process of gap junctional intercellular communication (GJIC). In this study we examined the role of GJ and GJIC in mechanically stimulated osteoblastic cells. Following fluid flow stimulation, we quantified prostaglandin E2 (PGE2) (oscillatory flow) and cytosolic calcium (Ca2+) (oscillatory and steady flow) responses in ROS 17/2.8 cells and a derivative of these cells expressing antisense cDNA for the gap junction protein connexin 43 (RCx16) possessing significantly different levels of GJIC. We found that the ROS17/2.8 cells possessing increased GJIC also exhibited increased PGE2 release to the supernatant following oscillatory fluid flow stimulation in comparison to coupling-decreased RCx16 cells. Interestingly, we found that neither osteoblastic cell line responded to oscillatory or steady fluid flow stimulation with an increase in Ca2+. Thus, our results suggest that GJ and GJIC may be important in the mechanotransduction mechanisms by which PGE2 is mechanically induced in osteoblastic cells independent of Ca2+.

Original languageEnglish (US)
Pages (from-to)350-356
Number of pages7
JournalBone
Volume32
Issue number4
DOIs
StatePublished - Apr 1 2003
Externally publishedYes

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Gap Junctions
Dinoprostone
Calcium
Bone and Bones
Connexin 43
Connexins
Magnetic Fields
Ion Channels
Names
Signal Transduction
Complementary DNA
Hormones
Ions

ASJC Scopus subject areas

  • Physiology
  • Hematology

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Fluid flow-induced prostaglandin E2 response of osteoblastic ROS 17/2.8 cells is gap junction-mediated and independent of cytosolic calcium. / Saunders, M. M.; You, J.; Zhou, Z.; Li, Z.; Yellowley-genetos, Clare E; Kunze, E. L.; Jacobs, C. R.; Donahue, H. J.

In: Bone, Vol. 32, No. 4, 01.04.2003, p. 350-356.

Research output: Contribution to journalArticle

Saunders, M. M. ; You, J. ; Zhou, Z. ; Li, Z. ; Yellowley-genetos, Clare E ; Kunze, E. L. ; Jacobs, C. R. ; Donahue, H. J. / Fluid flow-induced prostaglandin E2 response of osteoblastic ROS 17/2.8 cells is gap junction-mediated and independent of cytosolic calcium. In: Bone. 2003 ; Vol. 32, No. 4. pp. 350-356.
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