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A more recent version of this article appeared on July 1, 2005
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Submitted on October 19, 2004
Revised on March 18, 2005
Accepted on April 8, 2005
Departments of *Biochemistry and Radiology, University of Texas Health Science Center, San Antonio, TX 78229-3900; Department of Oral Biology, School of Dentistry, University of Missouri, Kansas City, MO 64108
Monitoring Editor: Asma Nusrat
Mechanosensing bone osteocytes express large amounts of connexin (Cx) 43, the component of gap junctions, yet gap junctions are only active at the small tips of their dendritic processes, suggesting another function for Cx43. Both primary osteocytes and the osteocyte-like MLO-Y4 cells respond to fluid flow shear stress by releasing intracellular prostaglandin E2 (PGE2) (Cheng et al., 2001a; Klein-Nulend et al., 1995). Cells plated at lower densities release more PGE2 than cells plated at higher densities. This response was significantly reduced by antisense to Cx43 and by the gap junction and hemichannel inhibitors, 18 
-glycyrrhetinic acid (-GA) and carbenoxolone, even in cells without physical contact, suggesting the involvement of Cx43-hemichannels. Inhibitors of other channels, such as the purinergic receptor P2X7 and the prostaglandin transporter PGT, had no effect on PGE2 release. Cell surface biotinylation analysis showed that surface expression of Cx43 was increased by shear stress. Together, these results suggest fluid flow shear stress induces the translocation of Cx43 to the membrane surface and that unapposed hemichannels formed by Cx43 serve as a novel portal for the release of PGE2 in response to mechanical strain.
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