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Related Concept Videos

Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Essential Minerals for Bone Health01:31

Essential Minerals for Bone Health

The minerals contained in all of the food we consume are essential for our organ systems. However, certain essential minerals, such as calcium, phosphorus, magnesium, manganese, and fluoride, largely affect bone health.
Calcium and Phosphorus
Calcium is a critical component of bones, especially in the form of calcium phosphate and calcium carbonate. Since the body cannot make calcium, it must be obtained from the diet. However, calcium cannot be absorbed from the small intestine without...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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 Remodeling and Repair01:31

Bone Remodeling and Repair

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...
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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Related Experiment Video

Updated: May 26, 2026

Bone Conditioned Medium: Preparation and Bioassay
07:18

Bone Conditioned Medium: Preparation and Bioassay

Published on: July 8, 2015

CCN3: lactational bone booster.

Nathan Xu1, Kyle Yang1, Mengjie Wang2,3

  • 1USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, USA.

Cell & Bioscience
|December 29, 2024
PubMed
Summary
This summary is machine-generated.

A newly discovered brain-bone axis reveals that cellular communication network factor 3 (CCN3) from specific neurons supports bone health in lactating mothers. This hormone is crucial for bone formation and offspring survival during nursing.

Keywords:
ARHERα/Kiss1 neuronsBone formationBrain-breast-bone axisCCN3Lactation

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Area of Science:

  • Endocrinology
  • Neuroscience
  • Skeletal Biology

Background:

  • Mammalian reproduction necessitates significant calcium transfer from mother to offspring via milk.
  • Lactation involves a complex brain-breast-bone circuit regulating hormones, calcium intake, and bone metabolism.
  • Traditionally, bone resorption driven by parathyroid hormone-related protein and low estrogen was considered the primary calcium source for milk.

Purpose of the Study:

  • To investigate novel mechanisms regulating the maternal skeleton during lactation.
  • To identify new signaling pathways within the brain-bone axis controlling calcium homeostasis and bone formation during nursing.
  • To elucidate the role of specific neuronal factors in supporting bone health and offspring survival.

Main Methods:

  • Parabiosis experiments
  • In vivo micro-computed tomography (µCT)
  • Bone transplantation assays
  • Cell culture and differentiation studies
  • Mouse genetic models
  • Pharmacological interventions
  • Hepatic viral transduction
  • Sequencing analysis

Main Results:

  • Cellular communication network factor 3 (CCN3), originating from ARHERα/Kiss1 neurons, acts as an osteogenic hormone.
  • CCN3 expression in these neurons is lactation-specific and crucial for bone maintenance.
  • CCN3 promotes skeletal stem cell activity, bone remodeling, and fracture repair in both young and aged mice.
  • Knockdown of CCN3 in lactating mothers led to severe bone loss and impaired offspring survival.

Conclusions:

  • A novel brain-bone axis involving lactation-specific CCN3 expression in ARHERα/Kiss1 neurons has been identified.
  • This CCN3-mediated pathway is essential for sustaining maternal bone integrity and ensuring offspring viability during lactation.
  • This discovery offers new insights into the evolutionary adaptations supporting mammalian reproduction and skeletal health.