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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 bone...

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Related Experiment Video

Updated: Jun 19, 2026

Establishment of a Surgically-induced Model in Mice to Investigate the Protective Role of Progranulin in Osteoarthritis

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Impaired osteoblast function in GPRC6A null mice.

Min Pi¹, Lishu Zhang, Shu-Feng Lei

¹Department of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. mpi@uthsc.edu

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research

|October 31, 2009

Summary

The GPRC6A receptor plays a crucial role in bone health. Its absence in mice leads to reduced bone mineral density and impaired osteoblast function, suggesting GPRC6A is vital for bone mineralization.

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Last Updated: Jun 19, 2026

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Published on: December 18, 2019

Area of Science:

Molecular Biology
Endocrinology
Bone Biology

Background:

G protein-coupled receptor 6A (GPRC6A) is an orphan receptor sensing amino acids, osteocalcin, and cations.
GPRC6A knockout mice display metabolic issues, including osteopenia.

Purpose of the Study:

To determine if GPRC6A deficiency directly impacts osteoblast function and bone metabolism.
To investigate the association between GPRC6A gene variations and bone mineral density in humans.

Main Methods:

Examined primary osteoblasts and bone marrow stromal cells from GPRC6A knockout mice.
Utilized siRNA to knock down GPRC6A in MC3T3 osteoblasts.
Analyzed GPRC6A gene polymorphisms in relation to bone mineral density in 1000 Caucasians.

Main Results:

GPRC6A knockout mice showed decreased bone mineral density and reduced expression of key bone markers (osteocalcin, ALP, OPG, Runx2-II).
Osteoblasts and BMSCs from knockout mice had impaired response to calcium, reduced alkaline phosphatase, and defective mineralization.
GPRC6A knockdown reduced calcium-stimulated ERK activity in osteoblasts.
GPRC6A gene polymorphisms were significantly linked to human spine bone mineral density.

Conclusions:

GPRC6A directly regulates osteoblast-mediated bone mineralization.
GPRC6A may mediate the anabolic effects of amino acids, osteocalcin, and divalent cations in bone.
GPRC6A is a potential therapeutic target for bone disorders.