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Related Experiment Video

Updated: Jun 18, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

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Published on: May 31, 2016

Elevated BMPR2 expression amplifies osteoblast differentiation in ankylosing spondylitis.

Sungsin Jo¹, Seung Hoon Lee¹, Chanhyeok Jeon^1,2

¹Hanyang University Institute for Rheumatology Research (HYIRR), Seoul, Korea.

Journal of Rheumatic Diseases

|September 22, 2023

Summary

Bone morphogenetic protein receptor type 2 (BMPR2) is elevated in ankylosing spondylitis (AS) osteoprogenitors, suggesting a role in disease progression. AS cells show enhanced response to bone morphogenetic protein 2 (BMP2) signaling.

Keywords:

Ankylosing spondylitis Bone morphogenetic protein 2 Bone morphogenetic protein receptor type 2 Osteoprogenitors

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Published on: March 18, 2019

Area of Science:

Biomedical research
Skeletal biology
Inflammatory diseases

Background:

Ankylosing spondylitis (AS) involves radiographic changes linked to bone morphogenetic protein receptor type 2 (BMPR2).
The precise role of BMPR2 and bone morphogenetic protein 2 (BMP2) signaling in AS osteoprogenitors remains unclear.

Purpose of the Study:

To investigate BMPR2 expression in AS.
To examine the BMP2-mediated signaling pathway in AS osteoprogenitors.

Main Methods:

RNA sequencing of osteoprogenitors (OPs) from healthy controls (HC) and AS patients.
Validation using immunohistochemistry and assessment of osteogenic differentiation potential.

Main Results:

BMPR2 expression was significantly higher in AS-OPs and facet joint tissues compared to HCs.
AS-OPs demonstrated a heightened response to BMP2-induced osteogenic differentiation and RUNX2 expression.

Conclusions:

Elevated BMPR2 expression in AS facet joints suggests its involvement in the disease.
BMPR2 may contribute to AS pathogenesis via BMP2-mediated pathways.