The role of actin cytoskeleton in oscillatory fluid flow-induced signaling in MC3T3-E1 osteoblasts

The role of actin cytoskeleton in oscillatory fluid flow-induced signaling in MC3T3-E1 osteoblasts

Fluid flow due to loading in bone is a potent mechanical signal that may play an important role in bone adaptation to its mechanical environment. Previous in vitro studies of osteoblastic cells revealed that the upregulation of cyclooxygenase-2 (COX-2) and c-fos induced by steady fluid flow depends...

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Bibliographic Details
Published in:American Journal of Physiology: Cell Physiology Vol. 292; no. 5; p. C1830
Main Authors: Malone, Amanda M D, Batra, Nikhil N, Shivaram, Giri, Kwon, Ron Y, You, Lidan, Kim, Chi Hyun, Rodriguez, Joshua, Jair, Kai, Jacobs, Christopher R
Format: Journal Article
Language:English
Published: United States 01-05-2007
Subjects:
3T3 Cells
Actins - metabolism
Animals
Biomechanical Phenomena
Calcium - metabolism
Cell Shape
Cytochalasin D - pharmacology
Cytoskeleton - drug effects
Cytoskeleton - metabolism
Dinoprostone - metabolism
Endoplasmic Reticulum - metabolism
Mechanotransduction, Cellular - drug effects
Mice
Osteoblasts - drug effects
Osteoblasts - metabolism
Pulsatile Flow
Stress Fibers - metabolism
Stress, Mechanical
Up-Regulation
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Summary:Fluid flow due to loading in bone is a potent mechanical signal that may play an important role in bone adaptation to its mechanical environment. Previous in vitro studies of osteoblastic cells revealed that the upregulation of cyclooxygenase-2 (COX-2) and c-fos induced by steady fluid flow depends on a change in actin polymerization dynamics and the formation of actin stress fibers. Exposing cells to dynamic oscillatory fluid flow, the temporal flow pattern that results from normal physical activity, is also known to result in increased COX-2 expression and PGE(2) release. The purpose of this study was to determine whether dynamic fluid flow results in changes in actin dynamics similar to steady flow and to determine whether alterations in actin dynamics are required for PGE(2) release. We found that exposure to oscillatory fluid flow did not result in the development of F-actin stress fibers in MC3T3-E1 osteoblastic cells and that inhibition of actin polymerization with cytochalasin D did not inhibit intracellular calcium mobilization or PGE(2) release. In fact, PGE(2) release was increased threefold in the polymerization inhibited cells and this PGE(2) release was dependent on calcium release from the endoplasmic reticulum. This was in contrast to the PGE(2) release that occurs in normal cells, which is independent of calcium flux from endoplasmic reticulum stores. We suggest that this increased PGE(2) release involves a different molecular mechanism perhaps involving increased deformation due to the compromised cytoskeleton.
ISSN:0363-6143
DOI:10.1152/ajpcell.00352.2005