Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Osteoclasts in Bone Remodeling

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...

Bone Remodeling

Bone Remodeling

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.

Hormones and Bone Tissue

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...

Transducer Mechanism: Enzyme-Linked Receptors

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:

Regulation of Metabolism

Regulation of Metabolism

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...

Global Regulatory Systems

Global Regulatory Systems

Global regulatory systems in bacteria enable rapid and coordinated responses to environmental changes by integrating sensory inputs with gene expression, ensuring efficient adaptation to fluctuating conditions. Key global regulatory mechanisms include regulons, two-component systems, sigma factors, and secondary messengers.Regulons and Global RegulatorsA regulon is a collection of genes and operons controlled by a common global regulator. These regulators enable bacteria to prioritize resource...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Impaired glycoRNA biogenesis in metabolic-dysfunction associated steatotic liver disease.

Journal of hepatology·2026

Same author

The response to danger: Is it in your bones?

Neuron·2026

Same author

Dasatinib and quercetin prevent alveolar bone loss in aged mice.

Journal of periodontology·2026

Same author

Dissecting the effects of <sup>223</sup>Radium on the bone microenvironment.

Acta pharmaceutica Sinica. B·2025

Same author

Potential Biological and Genetic Links Between Dementia and Osteoporosis: A Scoping Review.

Geriatrics (Basel, Switzerland)·2025

Same author

YAP/TAZ are crucial regulators of macrophage-mediated pulmonary inflammation and fibrosis after bleomycin-induced injury.

The European respiratory journal·2025

Search research articles

Related Experiment Video

Updated: Jul 5, 2026

Osteoclast Derivation from Mouse Bone Marrow

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Cocaine and amphetamine-regulated transcript may regulate bone remodeling as a circulating molecule.

Manvendra K Singh¹, Florent Elefteriou, Gerard Karsenty

¹Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, 701 West 168th Street, New York, New York 10032, USA.

|May 3, 2008

Summary

Cocaine- and amphetamine-regulated transcript (CART) influences bone mass by affecting osteoclast numbers. Circulating CART, not brain CART, appears to be key for regulating bone remodeling and rescuing low bone mass.

More Related Videos

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Related Experiment Videos

Last Updated: Jul 5, 2026

Osteoclast Derivation from Mouse Bone Marrow

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Area of Science:

Endocrinology
Bone Biology
Neuroendocrinology

Background:

Leptin regulates bone mass through mediators like Cocaine- and amphetamine-regulated transcript (CART).
CART is expressed in the brain and peripheral tissues, including the pituitary and pancreatic islets.
CART deficiency in Cart(-/-) mice leads to low bone mass due to increased osteoclast numbers.

Purpose of the Study:

To investigate the role of CART in bone mass regulation.
To determine whether CART acts centrally or peripherally to influence bone remodeling.
To explore therapeutic strategies for low bone mass phenotypes related to CART.

Main Methods:

Administration of recombinant CART into the third ventricle of Cart(-/-) mice.
Analysis of bone mass and osteoclast number in Cart(-/-) mice treated centrally.
Generation and analysis of transgenic mice with elevated circulating CART levels.
Assessment of the ability of increased circulating CART to rescue the low bone mass phenotype.

Main Results:

Central delivery of CART did not rescue the low bone mass phenotype in Cart(-/-) mice, though it impacted fat pad mass.
Transgenic mice with a 2-fold increase in circulating CART exhibited high bone mass due to decreased osteoclast numbers.
Elevated circulating CART levels in transgenic mice rescued the low bone mass phenotype of Cart(-/-) mice.

Conclusions:

CART's role in bone remodeling regulation appears to be primarily as a circulating molecule rather than a neuropeptide.
Peripheral actions of CART are more significant for maintaining bone mass than central actions.
Targeting circulating CART levels may offer a therapeutic approach for bone loss conditions.