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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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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.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Bone Remodeling01:40

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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.
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

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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Bones contain a relatively small number of cells entrenched in a matrix of organic and inorganic components. Although bone cells compose only a small amount of the bone volume, they are crucial to its function. Four types of cells are found within the bone tissue— osteoblasts, osteocytes, osteogenic cells, and osteoclasts.
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Related Experiment Video

Updated: May 27, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Osterix is regulated by Erk1/2 during osteoblast differentiation.

You Hee Choi1, Young-Mi Gu, Jae-Wook Oh

  • 1College of Pharmacy and Research Institute of Drug Development, Chonnam National University, Gwangju 500-757, Republic of Korea.

Biochemical and Biophysical Research Communications
|November 8, 2011
PubMed
Summary

The Erk1/2 pathway enhances osteoblast differentiation by stabilizing Osterix (Osx) protein and boosting its transcriptional activity. This discovery clarifies a key signaling mechanism in bone formation and homeostasis.

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Osteoclast Derivation from Mouse Bone Marrow
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Last Updated: May 27, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

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Published on: February 28, 2017

Osteoclast Derivation from Mouse Bone Marrow
06:17

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Bone Biology

Background:

  • Osterix (Osx) is a critical transcription factor for osteoblast differentiation and bone homeostasis.
  • Mitogen-activated protein (MAP) kinases, including Erk1/2, are involved in cellular signaling pathways.
  • The precise interaction between Osx and Erk1/2 in osteoblast differentiation remains unclear.

Purpose of the Study:

  • To investigate the relationship between Osterix and Erk1/2 signaling during osteoblast differentiation.
  • To elucidate the role of the MAPK pathway in regulating Osterix protein levels and transcriptional activity.

Main Methods:

  • Utilized overexpression of constitutively active MEK to activate Erk.
  • Employed U0126, a MEK inhibitor, to block Erk activation.
  • Assessed changes in Osterix mRNA and protein levels, as well as its transcriptional activity.

Main Results:

  • Erk activation increased both mRNA and protein levels of Osterix.
  • Constitutively active MEK enhanced Osterix transcriptional activity.
  • MEK inhibition suppressed Osterix protein levels and transcriptional activity.
  • Erk activation led to the stabilization of Osterix protein.

Conclusions:

  • Erk1/2 signaling positively regulates Osterix during osteoblast differentiation.
  • Erk1/2 increases Osterix protein stability and enhances its transcriptional function.
  • This signaling axis is crucial for maintaining bone homeostasis and formation.