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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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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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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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Hormones and Bone Tissue01:17

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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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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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Regulation of Metabolism01:19

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Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Related Experiment Video

Updated: Jun 5, 2025

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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Rc3h1 negatively regulates osteoclastogenesis by limiting energy metabolism.

Liuyuan Chen1, Yuangang Su1,2, Chaofeng Wang1,2

  • 1Guangxi Key Laboratory of Regenerative Medicine, Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China.

Theranostics
|December 11, 2024
PubMed
Summary

The RNA-binding protein Rc3h1 limits iron absorption and mitochondrial respiration in bone-resorbing osteoclasts. Targeting the Rc3h1/Tfr1 pathway may treat bone-loss diseases.

Keywords:
Rc3h1Tfr1mitochondriaosteoclastosteoporosis

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Last Updated: Jun 5, 2025

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Area of Science:

  • Cell Biology
  • Bone Biology
  • Metabolism

Background:

  • Osteoclasts are crucial for bone resorption, requiring significant mitochondrial respiration.
  • The RNA-binding protein Rc3h1 regulates mRNA homeostasis, but its role in osteoclast iron metabolism and mitochondrial function is unknown.

Purpose of the Study:

  • To investigate the role of Rc3h1 in regulating osteoclast function, iron metabolism, and mitochondrial respiration.
  • To identify the downstream targets of Rc3h1 involved in these processes.

Main Methods:

  • Generated Rc3h1-deficient mice and osteoclasts for in vitro and in vivo studies.
  • Evaluated bone mass, osteoclast activity, differentiation, and bone resorption.
  • Assessed cellular iron content and mitochondrial function.
  • Investigated Rc3h1 target genes and their role in mediating Rc3h1 effects.

Main Results:

  • Rc3h1 deficiency in mice led to low bone mass and enhanced osteoclast activation.
  • Rc3h1 post-transcriptionally repressed transferrin receptor 1 (Tfr1) expression, limiting iron absorption and mitochondrial respiration.
  • Inhibition of Tfr1 in Rc3h1-deficient osteoclasts reduced excessive osteoclast formation and mitochondrial respiration.

Conclusions:

  • Rc3h1 negatively regulates osteoclast activation by controlling iron resorption and mitochondrial respiration.
  • The Rc3h1/Tfr1 axis is a potential therapeutic target for bone-loss diseases.