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J. Biol. Chem., Vol. 278, Issue 6, 4082-4086, February 7, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/6/4082    most recent M205880200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jørgensen, N. R. Articles by Steinberg, T. H. Search for Related Content PubMed PubMed Citation Articles by Jørgensen, N. R. Articles by Steinberg, T. H. Social Bookmarking                      What's this?

Activation of L-type Calcium Channels Is Required for Gap Junction-mediated Intercellular Calcium Signaling in Osteoblastic Cells^*

Niklas Rye Jørgensen^§, Stefan Cuoni Teilmann, Zanne Henriksen, Roberto Civitelli^¶, Ole Helmer Sørensen, and Thomas H. Steinberg^¶

From the  Osteoporosis and Metabolic Bone Unit, Department of Endocrinology, Copenhagen University Hospitals, Copenhagen Hospital Corporation DK-2650 Hvidovre, Denmark and the ^¶ Department of Internal Medicine, Washington University School of Medicine, Washington University, St. Louis, Missouri 63110

The propagation of mechanically induced intercellular calcium waves (ICW) among osteoblastic cells occurs both by activation of P2Y (purinergic) receptors by extracellular nucleotides, resulting in "fast" ICW, and by gap junctional communication in cells that express connexin43 (Cx43), resulting in "slow" ICW. Human osteoblastic cells transmit intercellular calcium signals by both of these mechanisms. In the current studies we have examined the mechanism of slow gap junction-dependent ICW in osteoblastic cells. In ROS rat osteoblastic cells, gap junction-dependent ICW were inhibited by removal of extracellular calcium, plasma membrane depolarization by high extracellular potassium, and the L-type voltage-operated calcium channel inhibitor, nifedipine. In contrast, all these treatments enhanced the spread of P2 receptor-mediated ICW in UMR rat osteoblastic cells. Using UMR cells transfected to express Cx43 (UMR/Cx43) we confirmed that nifedipine sensitivity of ICW required Cx43 expression. In human osteoblastic cells, gap junction-dependent ICW also required activation of L-type calcium channels and influx of extracellular calcium.

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