A FAK/HDAC5 signaling axis controls osteocyte mechanotransduction
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Osteocytes, cells ensconced within mineralized bone matrix, are the primary skeletal mechanosensors. Osteocytes sense mechanical cues by changes in fluid flow shear stress (FFSS) across their dendritic projections. Loading-induced reductions of osteocytic Sclerostin (encoded by Sost) expression stimulates new bone formation. However, the molecular steps linking mechanotransduction and Sost suppression remain unknown. Here, we report that class IIa histone deacetylases (HDAC4 and HDAC5) are required for loading-induced Sost suppression and bone formation. FFSS signaling drives class IIa HDAC nuclear translocation through a signaling pathway involving direct HDAC5 tyrosine 642 phosphorylation by focal adhesion kinase (FAK), a HDAC5 post-translational modification that controls its subcellular localization. Osteocyte cell adhesion supports FAK tyrosine phosphorylation, and FFSS triggers FAK dephosphorylation. Pharmacologic FAK catalytic inhibition reduces Sost mRNA expression in vitro and in vivo. These studies demonstrate a role for HDAC5 as a transducer of matrix-derived cues to regulate cell type-specific gene expression.
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FFSS induces the disruption of the FAK-integrin complex, thereby inhibiting HDAC4/5, a negative regulator of SOST expression in osteocytes modulated by PTH treatment.
“Recently, Sato et al.20,44 showed that FFSS induces the disruption of the FAK-integrin complex, thereby inhibiting histone deacetylase 4/5 (HDAC4/5), a negative regulator of SOST expression in osteocytes45 modulated by parathyroid hormone (PTH) treatment.46”
From Bone remodeling: an operational process ensuring survival and bone mechanical competence (2022) · cites this paper as [44]
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Mechanical regulation of bone remodeling
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- Authors
- Sato, T., Verma, S., Andrade, C. D. C., Omeara, M., Campbell, N., Wang, J. S., Cetinbas, M., Lang, A., Ausk, B. J., Brooks, D. J., Sadreyev, R. I., Kronenberg, H. M., Lagares, D., Uda, Y., Pajevic, P. D., Bouxsein, M. L., Gross, T. S., & Wein, M. N.
- Affiliations
- Harvard University (US)
- University of Washington (US)
- Beth Israel Deaconess Medical Center (US)
- Boston University (US)
- Broad Institute (US)
- Corresponding author
- Wein, Marc N.
- ORCID
- Venue
- Nature Communications
- Published
- 2020-07-01
- Volume
- 11
- Issue
- 1
- Pages
- 3282-3282
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC7329900
- OpenAlex
- W3040185189
- Cited by
- 86
- References
- 105
- Citations by year
- 2026: 8 · 2025: 13 · 2024: 13 · 2023: 13 · 2022: 20 · 2021: 16 · 2020: 3
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR067285, AR066261)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- osteocytes, mechanotransduction, fluid shear stress, focal adhesion kinase, HDAC5, HDAC4, class IIa histone deacetylases, sclerostin, tyrosine phosphorylation, bone formation, bone loading, cell adhesion, nuclear translocation
- MeSH terms
- Animals, Cell Line, Histone Deacetylases, Humans, Mice, Inbred C57BL, Osteocytes, Osteogenesis, Phosphorylation, Signal Transduction, Mice, Knockout, Gene Expression Profiling, Mechanotransduction, Cellular, Cell Line, Tumor, Focal Adhesion Protein-Tyrosine Kinases
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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