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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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Regulation of Angiogenesis and Blood Supply01:24

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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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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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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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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.
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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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Related Experiment Video

Updated: Mar 10, 2026

Development of a Human Preclinical Model of Osteoclastogenesis from Peripheral Blood Monocytes Co-cultured with Breast Cancer Cell Lines
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Osteoblasts secrete Cxcl9 to regulate angiogenesis in bone.

Bin Huang1, Wenhao Wang1, Qingchu Li1

  • 1Academy of Orthopedics, Guangdong Province, Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou 510630, China.

Nature Communications
|December 15, 2016
PubMed
Summary

Osteoblasts secrete Cxcl9, an angiostatic factor that inhibits blood vessel formation and bone growth by blocking vascular endothelial growth factor. Targeting Cxcl9 may treat bone loss diseases.

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Area of Science:

  • Bone biology
  • Angiogenesis
  • Cellular communication

Background:

  • Osteoblast-endothelial cell (EC) communication is crucial for bone remodeling.
  • Molecular mechanisms regulating this crosstalk are not fully understood.

Purpose of the Study:

  • To identify molecular factors involved in osteoblast-EC communication.
  • To elucidate the role of these factors in bone angiogenesis and osteogenesis.

Main Methods:

  • Identification of Cxcl9 as an osteoblast-secreted factor.
  • In vitro and in vivo experiments using mouse bone models.
  • Analysis of vascular endothelial growth factor (VEGF) interactions.
  • Investigation of mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway.

Main Results:

  • Cxcl9, secreted by osteoblasts, acts as an angiostatic factor.
  • Cxcl9 inhibits angiogenesis and osteogenesis by interfering with VEGF binding to ECs and osteoblasts.
  • mTORC1 signaling upregulates Cxcl9 expression via STAT1, enhancing STAT1 binding to the Cxcl9 promoter.

Conclusions:

  • Osteoblast-derived Cxcl9 plays a critical role in regulating bone angiogenesis and osteogenesis.
  • Targeting Cxcl9 presents a potential therapeutic strategy to enhance bone angiogenesis and combat bone loss.