Related Experiment Video

Updated: May 7, 2026

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

9.9K

NF-κB RelB negatively regulates osteoblast differentiation and bone formation

Zhenqiang Yao1, Yanyun Li, Xiaoxiang Yin

  • 1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|October 12, 2013
PubMed

Insights

Nuclear factor-kappa B (NF-κB) RelB protein inhibits bone formation. RelB deficiency in mice leads to increased bone mass and enhanced bone repair, suggesting RelB inhibition for treating bone loss.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Bone Biology

Background:

  • Nuclear factor-kappa B (NF-κB) signaling pathways play critical roles in bone metabolism.
  • While RelA-mediated NF-κB signaling is known to affect bone formation, the role of NF-κB RelB in this process remains less understood.
  • Previous studies on RelB's role in bone formation utilized complex models and did not elucidate underlying molecular mechanisms.

Purpose of the Study:

  • To investigate the role of NF-κB RelB in regulating bone mass and formation.
  • To elucidate the molecular mechanisms by which RelB influences osteoblast differentiation and bone repair.

Main Methods:

  • Utilized RelB knockout (RelB(-/-)) mice to study age-related bone mass changes.
  • Assessed mesenchymal progenitor cell (MPC) proliferation and osteoblast (OB) differentiation in vitro.
  • Analyzed the expression of Runt-related transcription factor 2 (Runx2) in RelB(-/-) cells.
  • Investigated the direct interaction of RelB with the Runx2 promoter.
  • Evaluated bone formation in a murine tibial bone defect model using RelB(-/-) bone-derived MPCs.

Main Results:

  • RelB(-/-) mice exhibited increased trabecular bone mass and enhanced bone formation with age.
  • RelB(-/-) bone marrow stromal cells showed increased proliferation and enhanced OB differentiation.
  • RelB(-/-) cells displayed increased expression of the osteoblastogenic transcription factor Runx2.
  • RelB was found to directly target and inhibit the activation of the Runx2 promoter.
  • Bone defects healed more rapidly in mice injected with RelB(-/-) MPCs compared to wild-type controls.

Conclusions:

  • NF-κB RelB negatively regulates bone mass during aging.
  • RelB limits bone formation in healing bone defects.
  • Inhibition of RelB presents a potential therapeutic strategy for reducing age-related bone loss and improving bone repair.
Keywords:
BONE FORMATIONMESENCHYMAL PROGENITOR CELLSNF-κBOSTEOBLASTSRELB

More Related Videos

A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro07:03

A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro

Published on: June 16, 2022

6.6K
Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

5.3K

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
7.7K
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...
3.9K
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
7.0K
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
6.7K
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

2.0K
Bone Remodeling01:40

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.
34.4K