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Related Experiment Video

Updated: Jun 24, 2025

Preparation Of Gushukang GSK Granules for In Vivo and In Vitro Experiments

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Published on: May 9, 2019

GREM2 inactivation increases trabecular bone mass in mice.

Karin H Nilsson¹, Petra Henning², Jianyao Wu²

¹Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. karin.nilsson.2@gu.se.

Scientific Reports

|June 5, 2024

Summary

This summary is machine-generated.

Genetic variants in GREM2 are linked to osteoporosis. Inactivating GREM2 in mice increased bone density and stimulated bone-forming cells, suggesting GREM2 as a potential therapeutic target for osteoporosis treatment.

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Area of Science:

Bone biology and genetics
Skeletal disease research

Background:

Osteoporosis is a prevalent skeletal disorder causing fractures and reduced quality of life.
Genetic studies link the FMN2/GREM2 locus to trabecular bone mineral density and fracture risk.
GREM2 functions as a bone morphogenetic protein (BMP) antagonist.

Purpose of the Study:

To investigate if GREM2 is the causal gene for fracture risk associated with the FMN2/GREM2 locus.
To explore the role of GREM2 in bone metabolism and osteoblast differentiation.

Main Methods:

Utilized Grem2-deficient mice (Grem2-/- and Grem2+/-) for functional studies.
Analyzed bone mineral density (BMD), bone structure (trabecular and cortical thickness), and gene expression in osteoblasts.
Assessed the impact of Grem2 inactivation on osteoblast differentiation markers (Alp, Bglap, Sp7).

Main Results:

Grem2 is expressed in bone tissue, particularly in osteoblasts.
Partial Grem2 inactivation in female mice (Grem2+/-) increased trabecular BMD and bone mass.
Grem2 inactivation stimulated osteoblast differentiation and expression of key bone formation genes.
Complete Grem2 deletion affected mouse survival and growth.

Conclusions:

GREM2 plays a role in regulating trabecular bone mass.
GREM2 inactivation enhances osteoblast differentiation and bone formation.
GREM2 is a potential therapeutic target for increasing bone mass and preventing osteoporotic fractures.