IMR Press / FBL / Volume 7 / Issue 1 / DOI: 10.2741/A733

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Control of calcium entry in human fibroblasts by frequency-dependent electrical stimulation
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1 Department of Bioengineering, University of Illinois, Chicago, IL 60607
2 Department of Physics, Wellesley College, Wellesley, MA 02481
3 Department of Surgery, Harvard Medical School and Boston VA HealthCare System, West Roxbury, MA 02132
4 Departments of Biological Chemistry and Molecular Pharmacology and of Medicine, Harvard Medical School; Hematology Division, Brigham and Women's Hospital, Boston, MA 02115
Academic Editor:Jeremy Mao
Front. Biosci. (Landmark Ed) 2002, 7(1), 1–8;
Published: 1 January 2002
(This article belongs to the Special Issue Biomimetics and engineering of skeletal tissues)

Modulation of intracellular calcium ion concentration ((Ca2+)i) could be used to control cellular and molecular responses that are important in cell and tissue engineering. Electrical stimulation (ES) has been used to activate plasma membrane ion channels including Ca2+channels, and to induce changes in (Ca2+)i. Strong direct current (dc) ES depolarizes the membrane electrical potential (MEP) and, thereby, causes rapid increases in (Ca2+)i. Electrocoupling mechanisms that could control (Ca2+)i increases induced by modes of ES other than dc have not been elucidated, however. Here we report that 30 min of continuous exposure to a 1 or 10 Hz, 2 V/cm ES induces an (Ca2+)i increase by a ~ 6-fold (baseline 25 nM) in human fibroblasts in culture. In contrast, a 100 Hz, 2 V/cm ES causes no significant (Ca2+)i increase. Either depletion of Ca2+from the extracellular medium or incubation of cells with verapamil inhibits the (Ca2+)i increase, indicating that Ca2+ influx through verapamil-sensitive Ca2+channels is required for the (Ca2+)i increase induced by oscillatory ES. More intense ES by a 1 Hz or a dc 10 V/cm electric field causes a rapid 20 to 25-fold (Ca2+)i increase. We hypothesize that selective, partial activation of Ca2+channels is likely to mediate Ca2+influx. These results suggest that optimal ES could be used to control Ca2+entry and, thereby, regulate cellular calcium homeostasis without adversely affecting cell viability.

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