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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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 bone...
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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
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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 bone...

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Differentiation and Characterization of Osteoclasts from Human Induced Pluripotent Stem Cells
10:52

Differentiation and Characterization of Osteoclasts from Human Induced Pluripotent Stem Cells

Published on: March 22, 2024

Wdr5 is essential for osteoblast differentiation.

Eric D Zhu1, Marie B Demay, Francesca Gori

  • 1Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.

The Journal of Biological Chemistry
|January 19, 2008
PubMed
Summary
This summary is machine-generated.

WD repeat domain 5 (Wdr5) is crucial for osteoblast differentiation and bone formation. Suppressing Wdr5 inhibits key differentiation markers and impairs Wnt signaling, essential for bone development.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Wdr5 is developmentally expressed in osteoblasts.
  • Wdr5 accelerates osteoblast differentiation in vitro and in vivo.
  • Wdr5 is known to enhance canonical Wnt signaling in osteoblasts.

Purpose of the Study:

  • To determine if Wdr5 is essential for osteoblast differentiation.
  • To investigate the effects of Wdr5 suppression on the canonical Wnt signaling pathway.
  • To elucidate the role of Wdr5 in regulating osteoblast gene expression and matrix formation.

Main Methods:

  • Stable suppression of endogenous Wdr5 protein levels using plasmid-based small interfering RNAs in MC3T3-E1 cells.
  • Assessed osteoblast differentiation markers: alkaline phosphatase activity, Runx-2 and osteocalcin mRNA levels, and mineralized matrix formation.
  • Examined canonical Wnt signaling pathway components, including target gene expression (c-myc, sfrp2), beta-catenin levels, and Wnt expression.
  • Utilized chromatin immunoprecipitation to determine Wdr5 binding to target gene promoters.

Main Results:

  • Wdr5 suppression significantly inhibited osteoblast differentiation, reducing alkaline phosphatase activity, Runx-2 and osteocalcin mRNA, and matrix mineralization.
  • Wdr5 knockdown led to decreased histone H3 lysine 4 trimethylation, confirming Wdr5's role in this epigenetic modification.
  • Canonical Wnt signaling was impaired: c-myc expression decreased, sfrp2 expression increased, Wnt expression decreased, and nuclear beta-catenin levels were reduced.
  • Wdr5 was found to bind to the Wnt1 promoter and Wnt response elements of c-myc and Runx-2 promoters.

Conclusions:

  • Optimal Wdr5 levels are required for the induction of the osteoblast phenotype.
  • Wdr5 suppression interferes with the canonical Wnt signaling pathway at multiple stages.
  • Wdr5 plays a critical role in osteoblast differentiation through epigenetic regulation and Wnt signaling modulation.