ArticleAmerican journal of physiology. Cell physiology2007
The role of actin cytoskeleton in oscillatory fluid flow-induced signaling in MC3T3-E1 osteoblasts.
Article in American journal of physiology. Cell physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 86 citations in OpenAlex.
- Tracing Cellular Senescence in Bone: Time-Dependent Changes in Osteocyte Cytoskeleton Mechanics and Morphology.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Tracing Cellular Senescence in Bone: Time-Dependent Changes in Osteocyte Cytoskeleton Mechanics and Morphology.bioRxiv : the preprint server for biology · 2025Article
- Universal Biomaterial-on-Chip: a versatile platform for evaluating cellular responses on diverse biomaterial substrates.Journal of materials science. Materials in medicine · 2024Article
- Changes in interstitial fluid flow, mass transport and the bone cell response in microgravity and normogravity.Bone research · 2022Review
- The role of mechanobiology in bone and cartilage model systems in characterizing initiation and progression of osteoarthritis.APL bioengineering · 2022Review
- Liquid flow in scaffold derived from natural source: experimental observations and biological outcome.Regenerative biomaterials · 2022Article
- Low Intensity Pulsed Ultrasound for Bone Tissue Engineering.Micromachines · 2021Review
- Review
- Fluid shear stress and endothelial cells synergistically promote osteogenesis of mesenchymal stem cells via integrin β1-FAK-ERK1/2 pathway.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- Flow-induced mechanotransduction in skeletal cells.Biophysical reviews · 2019Review
- Impact of flow shear stress on morphology of osteoblast-like IDG-SW3 cells.Journal of bone and mineral metabolism · 2018Article
- Mechanically Loading Cell/Hydrogel Constructs with Low-Intensity Pulsed Ultrasound for Bone Repair.Tissue engineering. Part A · 2018Article
- Cellular fluid shear stress on implant surfaces-establishment of a novel experimental set up.International journal of implant dentistry · 2017Article
- Flowtaxis of osteoblast migration under fluid shear and the effect of RhoA kinase silencing.PloS one · 2017Article
- The molecular basis of bone mechanotransduction.Journal of musculoskeletal & neuronal interactions · 2016Review
- High-Frequency Acceleration: Therapeutic Tool to Preserve Bone following Tooth Extractions.Journal of dental research · 2016Article
- Experimental studies of bone mechanoadaptation: bridging in vitro and in vivo studies with multiscale systems.Interface focus · 2016Article
- Altered cytoskeletal organization characterized lethal but not surviving Brtl+/- mice: insight on phenotypic variability in osteogenesis imperfecta.Human molecular genetics · 2015Article
- Biomechanical forces in the skeleton and their relevance to bone metastasis: biology and engineering considerations.Advanced drug delivery reviews · 2014Review
- Mechanomics: an emerging field between biology and biomechanics.Protein & cell · 2014Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.