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Physiologic electrical stimulation provokes intracellular calcium increase mediated by phospholipase C activation in human osteoblasts
Author(s) -
Khatib Layla,
Golan David E.,
Cho Michael
Publication year - 2004
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.04-1814fje
Subject(s) - intracellular , stimulation , phospholipase c , calcium in biology , biophysics , verapamil , chemistry , calcium , receptor , phospholipase , microbiology and biotechnology , endocrinology , medicine , biology , biochemistry , enzyme , organic chemistry
Strong exogenous electrical stimulation (ES) can induce changes in intracellular calcium ion concentration ([Ca 2+ ] i ). It remains to be elucidated, however, whether physiologically relevant ES (e.g., 1–2 V/cm) could alter [Ca 2+ ] i . We have used fluorescence microscopy to quantify [Ca 2+ ] i changes in response to direct current (dc) ES in human fetal osteoblasts. Increases in [Ca 2+ ] i in response to 2 V/cm ES show a noticeable (20‐min) time delay, followed by a 45‐fold rise from the baseline of 40 nM to 1.8 μM. Treatment of cells with verapamil does not affect ES‐ induced [Ca 2+ ] i increases, but inhibition of phospholipase C (PLC) does prevent such increases, which suggests that receptor‐regulated release of Ca 2+ from intracellular stores is likely to be involved. Treatment of cells with the stretch‐activated cation channel (SACC) blocker Gd 3+ partially inhibits ES‐induced [Ca 2+ ] i increases, as does chelation of intracellular Ca 2+ . These results are consistent with a model in which physiologically relevant ES does not activate voltage‐gated Ca 2+ channels (VGCCs) directly, but rather stimulates PLC‐coupled cell surface receptors that induce [Ca 2+ ] i increases by activating IP 3 ‐dependent intracellular processes. The Ca 2+ influx that follows PLC activation is likely mediated by activation of mechanically operated SACCs.