TY - JOUR
T1 - Calcium signaling is required for ultrasound-stimulated aggrecan synthesis by rat chondrocytes
AU - Parvizi, Javad
AU - Parpura, Vladimir
AU - Greenleaf, James F.
AU - Bolander, Mark E.
N1 - Funding Information:
This work was supported by a Mayo Clinic Research Foundation Grant. The NORTH Scholarship, Newcastle upon Tyne, UK, also supported part of Dr. Parvizi's tenure. Dr. Parpuras' tenure was supported by the Whitehall Foundation. We thank Dr. Gobinda Sarkar, Mr. James T. Bronk, and Mr. Randall R. Kinnick for their assistance with experimentation and preparation of this manuscript.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2002
Y1 - 2002
N2 - Low-intensity ultrasound accelerates fracture healing in humans. In rat femur fracture models, ultrasound advanced healing is associated with increased proteoglycan expression. Here we report that ultrasound stimulation of primary rat chondrocytes elevated the intracellular concentration of calcium [Ca2+]i. The [Ca2+]i increase was rapid and transient at lower pressures (175-320 kPa), but rapid and sustained at higher ultrasound exposures (350-500 kPa). Chelating internal [Ca2+]i with 1,2-bis(2-aminophenoxy) ethane-N-N-N′,N′-tetraacetic acid (BAPTA-AM), stopping the Ca2+/ATP-ase induced mitochondrial release of [Ca2+]i with Thapsigargin, or removing [Ca2+]i from the medium with EGTA inhibited the stimulatory effects of ultrasound on proteoglycan synthesis. These results imply that ultrasound-stimulated synthesis of cell matrix proteoglycan, associated with accelerated fracture healing, is mediated by intracellular calcium signaling.
AB - Low-intensity ultrasound accelerates fracture healing in humans. In rat femur fracture models, ultrasound advanced healing is associated with increased proteoglycan expression. Here we report that ultrasound stimulation of primary rat chondrocytes elevated the intracellular concentration of calcium [Ca2+]i. The [Ca2+]i increase was rapid and transient at lower pressures (175-320 kPa), but rapid and sustained at higher ultrasound exposures (350-500 kPa). Chelating internal [Ca2+]i with 1,2-bis(2-aminophenoxy) ethane-N-N-N′,N′-tetraacetic acid (BAPTA-AM), stopping the Ca2+/ATP-ase induced mitochondrial release of [Ca2+]i with Thapsigargin, or removing [Ca2+]i from the medium with EGTA inhibited the stimulatory effects of ultrasound on proteoglycan synthesis. These results imply that ultrasound-stimulated synthesis of cell matrix proteoglycan, associated with accelerated fracture healing, is mediated by intracellular calcium signaling.
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U2 - 10.1016/S0736-0266(01)00069-9
DO - 10.1016/S0736-0266(01)00069-9
M3 - Article
C2 - 11853090
AN - SCOPUS:0036148989
SN - 0736-0266
VL - 20
SP - 51
EP - 57
JO - Journal of Orthopaedic Research
JF - Journal of Orthopaedic Research
IS - 1
ER -