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Related Concept Videos

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Related Experiment Video

Updated: Apr 23, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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HDAC5 controls MEF2C-driven sclerostin expression in osteocytes.

Marc N Wein1, Jordan Spatz, Shigeki Nishimori

  • 1Endocrine Unit, Massachusetts General Hospital, Boston, MA, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|October 2, 2014
PubMed
Summary

Histone deacetylase 5 (HDAC5) controls sclerostin production in bone cells. Inhibiting HDAC5 boosts sclerostin, impacting bone density and formation, revealing a new target for osteoporosis therapies.

Keywords:
EPIGENETICSOSTEOCYTESOSTEOPOROSISWNT/ß-CATENIN/LRPS

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Area of Science:

  • Molecular Biology
  • Bone Biology
  • Epigenetics

Background:

  • Osteocytes regulate bone remodeling via paracrine factors.
  • Sclerostin (SOST) inhibits bone formation and is an osteoporosis drug target.
  • Mechanisms controlling SOST expression are not well understood.

Purpose of the Study:

  • To investigate the role of histone deacetylase 5 (HDAC5) in regulating sclerostin (SOST) expression in osteocytes.
  • To elucidate the molecular mechanisms by which HDAC5 affects SOST levels and bone metabolism.

Main Methods:

  • Utilized a novel murine osteocytic cell line (Ocy454) for in vitro studies.
  • Employed HDAC5 knockdown (shRNA) and overexpression experiments.
  • Analyzed HDAC5 knockout mice for in vivo validation.
  • Performed chromatin immunoprecipitation (ChIP) to map transcription factor binding sites.
  • Assessed Wnt activity, bone density, and osteoblast function.

Main Results:

  • HDAC5 negatively regulates sclerostin levels in osteocytes.
  • HDAC5 deficiency in mice leads to increased SOST, reduced Wnt activity, lower bone density, and decreased bone formation.
  • HDAC5 directly inhibits the transcription factor MEF2C, a key regulator of SOST expression.
  • HDAC5 regulates a distal SOST enhancer by controlling MEF2C binding, histone acetylation, and corepressor recruitment.

Conclusions:

  • HDAC5 is a critical negative regulator of SOST gene expression in osteocytes.
  • The HDAC5-MEF2C axis controls sclerostin production and influences bone metabolism.
  • Targeting HDAC5 offers a potential therapeutic strategy for osteoporosis.