Fluid shear stress induces calcium transients in osteoblasts through depolarization of osteoblastic membrane |
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| Institution: | 1. The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi?an Jiaotong University, Xi?an 710049, China;2. Hong-hui Hospital, College of Medicine, Xi?an Jiaotong University, Xi?an 710054, China;1. Departments of Bioengineering, University of Pittsburgh, Pittsburgh, PA, United States;2. Cardiothoracic Surgery, University of Pittsburgh, Pittsburgh, PA, United States;3. Surgery, University of Pittsburgh, Pittsburgh, PA, United States;4. Center for Vascular Remodeling and Regeneration, University of Pittsburgh, Pittsburgh, PA, United States;5. McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, United States;1. Department of Biological Sciences, 1275 University Esplanade, Kent State University, Kent, OH 44242, USA;2. Department of Chemistry and Biochemistry, Kent State University, Kent, OH 44242, USA;3. J.A. Woollam Co., Inc., 645 M Street, Suite 102, Lincoln, NE 68508, USA;1. Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, the Netherlands;2. Institute for Complex Molecular Systems, Eindhoven University of Technology, Eindhoven, the Netherlands;3. Innovative Materials Laboratory, Italian Aerospace Research Centre, Capua, Italy;4. Department of Engineering, University of Cambridge, Cambridge, United Kingdom;1. Nano Medical Engineering Laboratory, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan;2. Emergent Bioengineering Materials Research Team, RIKEN Center for Emergent Matter Science, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan;1. Departments of Mechanical and Biomedical Engineering, Columbia University, New York, NY 10027, USA;2. Department of Materials, Imperial College London, London, UK |
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| Abstract: | Intracellular calcium transient (Ca2+]i transient) induced by fluid shear stress (FSS) plays an important role in osteoblastic mechanotransduction. Changes of membrane potential usually affect Ca2+]i level. Here, we sought to determine whether there was a relationship between membrane potential and FSS-induced Ca2+]i transient in osteoblasts. Fluorescent dyes DiBAC4(3) and fura-2 AM were respectively used to detect membrane potential and Ca2+]i. Our results showed that FSS firstly induced depolarization of membrane potential and then a transient rising of Ca2+]i in osteoblasts. There was a same threshold for FSS to induce depolarization of membrane potential and Ca2+]i transients. Replacing extracellular Na+ with tetraethylammonium or blocking stretch-activated channels (SACs) with gadolinium both effectively inhibited FSS-induced membrane depolarization and Ca2+]i transients. However, voltage-activated K+ channel inhibitor, 4-Aminopyridine, did not affect these responses. Removing extracellular Ca2+ or blocking of L-type voltage-sensitive Ca2+ channels (L-VSCCs) with nifedipine inhibited FSS-induced Ca2+]i transients in osteoblasts too. Quantifying membrane potential with patch clamp showed that the resting potential of osteoblasts was ?43.3 mV and the depolarization induced by FSS was about 44 mV. Voltage clamp indicated that this depolarization was enough to activated L-VSCCs in osteoblasts. These results suggested a time line of Ca2+ mobilization wherein FSS activated SACs to promote Na+ entry to depolarize membrane that, in turn, activated L-VSCCs and Ca2+ influx though L-VSCCs switched on Ca2+]i response in osteoblasts. |
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| Keywords: | Membrane potential Fluid shear stress Osteoblast |
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