ArticlePloS one2012
Focal adhesion kinase plays a role in osteoblast mechanotransduction in vitro but does not affect load-induced bone formation in vivo.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Regulation of cAMP levels in osteocytes by mechano-sensitive focal adhesion kinase and phosphodiesterase 8A.iScience · 2026Article
- Ciliary-Mediated Mechanotransduction in Skeletal Development and Diseases.Results and problems in cell differentiation · 2026Review
- Inhibition of focal adhesion kinase 2 results in a macrophage polarization shift to M2 which attenuates local and systemic inflammation and reduces heterotopic ossification after polysystem extremity trauma.Frontiers in immunology · 2023Article
- Inhibition of focal adhesion turnover prevents osteoblastic differentiation through β-catenin mediated transduction of pro-osteogenic substrate.Journal of biomedical materials research. Part B, Applied biomaterials · 2022Article
- Cytostatic Effects of Polyethyleneimine Surfaces on the Mesenchymal Stromal Cell Cycle.Polymers · 2022Article
- The Wnt pathway: An important control mechanism in bone's response to mechanical loading.Bone · 2021Review
- Low Intensity Pulsed Ultrasound for Bone Tissue Engineering.Micromachines · 2021Review
- RNAseq and RNA molecular barcoding reveal differential gene expression in cortical bone following hindlimb unloading in female mice.PloS one · 2021Article
- Pten deletion in Dmp1-expressing cells does not rescue the osteopenic effects of Wnt/β-catenin suppression.Journal of cellular physiology · 2020Article
- Dissecting the Effect of a 3D Microscaffold on the Transcriptome of Neural Stem Cells with Computational Approaches: A Focus on Mechanotransduction.International journal of molecular sciences · 2020Article
- A FAK/HDAC5 signaling axis controls osteocyte mechanotransduction.Nature communications · 2020Article
- Predicting gene expression using morphological cell responses to nanotopography.Nature communications · 2020Article
- Integrins in Osteocyte Biology and Mechanotransduction.Current osteoporosis reports · 2019Review
- Genetic Dissection of Trabecular Bone Structure with Mouse Intersubspecific Consomic Strains.G3 (Bethesda, Md.) · 2017Article
- Molecular stretching modulates mechanosensing pathways.Protein science : a publication of the Protein Society · 2017Review
- Lengthening primary cilia enhances cellular mechanosensitivity.European cells & materials · 2017Article
- Osteoblast-derived paracrine factors regulate angiogenesis in response to mechanical stimulation.Integrative biology : quantitative biosciences from nano to macro · 2016Article
- Tensile force on human macrophage cells promotes osteoclastogenesis through receptor activator of nuclear factor κB ligand induction.Journal of bone and mineral metabolism · 2016Article
- Modulation of unloading-induced bone loss in mice with altered ERK signaling.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Article
- Mechanotransduction in the endothelium: role of membrane proteins and reactive oxygen species in sensing, transduction, and transmission of the signal with altered blood flow.Antioxidants & redox signaling · 2014Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
A healthy skeleton relies on bone's ability to respond to external mechanical forces. The molecular mechanisms by which bone cells sense and convert mechanical stimuli into biochemical signals, a process known as mechanotransduction, are unclear. Focal adhesions play a critical role in cell survival, migration and sensing physical force. Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that controls focal adhesion dynamics and can mediate reparative bone formation in vivo and osteoblast mechanotransduction in vitro. Based on these data, we hypothesized that FAK plays a role in load-induced bone formation. To test this hypothesis, we performed in vitro fluid flow experiments and in vivo bone loading studies in FAK-/- clonal lines and conditional FAK knockout mice, respectively. FAK-/- osteoblasts showed an ablated prostaglandin E(2) (PGE(2)) response to fluid flow shear. This effect was reversed with the re-expression of wild-type FAK. Re-expression of FAK containing site-specific mutations at Tyr-397 and Tyr-925 phosphorylation sites did not rescue the phenotype, suggesting that these sites are important in osteoblast mechanotransduction. Interestingly, mice in which FAK was conditionally deleted in osteoblasts and osteocytes did not exhibit altered load-induced periosteal bone formation. Together these data suggest that although FAK is important in mechanically-induced signaling in osteoblasts in vitro, it is not required for an adaptive response in vivo, possibly due to a compensatory mechanism that does not exist in the cell culture system.
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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 Socratic graph.