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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...

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Toxicological Assays for Testing Effects of an Epigenetic Drug on Development, Fecundity and Survivorship of Malaria Mosquitoes

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Decreased bone resorption in Ezh2 myeloid cell conditional knockout mouse model.

Perry C Caviness^1,2, Dongzheng Gai³, Oxana P Lazarenko^1,2

¹Arkansas Children's Nutrition Center, Little Rock, Arkansas, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|June 5, 2023

Summary

Deleting enhancer of zeste homolog 2 (Ezh2) in myeloid cells boosts bone growth and formation. This epigenetic regulation offers potential treatments for bone loss disorders like osteoporosis.

Keywords:

Ezh2 bone resorption epigenetic osteoclast

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Area of Science:

Bone Biology
Epigenetics
Cellular Homeostasis

Background:

Osteoclasts regulate bone resorption, and understanding their development is key for treating bone disorders.
The role of the polycomb group protein enhancer of zeste homolog 2 (Ezh2) in bone cell development and homeostasis is not fully understood.

Purpose of the Study:

To investigate the role of Ezh2 in epigenetic regulation of osteoclastogenesis and bone homeostasis.
To determine the effects of conditional Ezh2 knockout in myeloid cells on bone growth and cellular composition.

Main Methods:

Conditional knockout (CKO) of Ezh2 in myeloid lineage macrophages using LysM-Cre and Ezh2flox/flox mice.
Analysis of bone mass, cellularity (macrophages, osteoblasts), and bone formation biomarkers (P1NP, osteocalcin).
Assessment of inflammatory markers and gene expression of osteoclast-suppressive genes (IRF8, MafB, Arg1) and H3K27me3 levels.

Main Results:

Conditional knockout of Ezh2 significantly increased postnatal bone growth in both male and female mice.
Ezh2 deletion in myeloid cells reduced macrophage numbers while increasing mature osteoblasts and bone formation markers.
Ezh2 deletion decreased the inflammatory milieu and led to increased expression of osteoclast-suppressive genes due to reduced H3K27me3 epigenetic marks.

Conclusions:

Ezh2 epigenetically regulates osteoclastogenesis and bone homeostasis.
Manipulation of Ezh2 in myeloid cells presents a potential therapeutic strategy for bone resorptive disorders like osteoporosis and arthritis.