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Distinctive Expression of Bone Metabolism-related Genes between PBMCs from Condylar Hyperplasia, Rheumatoid
Reza Amirzargar1, Gholamreza Shirani2, Shokoufeh Raisian3
1Department of Craniofacial Surgery, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran. amirzargar_reza@yahoo.com.
Abstract:
Bone morphogenetic proteins (BMPs) and wingless (Wnt) signaling molecules and their antagonists, such as sclerostin and noggin, have been identified to have different effects on bone metabolism. This research intended to evaluate the transcript levels of CTNNB1 (catenin beta 1protein), SOST (sclerostin protein), BMP4 (Bone Morphogenetic Protein 4 protein), and NOG (noggin protein) bone metabolism-related genes in peripheral blood mononuclear cells (PBMCs) from condylar hyperplasia (CH) patients in comparison to rheumatoid arthritis (RA), ankylosing spondylitis (AS), and healthy individuals. PBMCs were separated from blood samples of 10 patients with CH, AS, RA, and 10 healthy controls. SYBR Green real-time polymerase chain reaction (PCR) was used for quantitative analysis of CTNNB1, SOST, BMP4, and NOG messenger RNAs (mRNAs). The expression of CTNNB1 was significantly upregulated in CH and AS patients compared with healthy individuals and RA patients. The difference of SOST expression was not significant between all groups. The BMP4 expression was significantly downregulated in AS, CH, and RA patients compared with healthy controls. The NOG expression was downregulated in RA, AS, and CH groups, however, it was only significant in CH and RA patients compared with controls.CH and AS patients were distinguished from RA by the upregulatedCTNNB1 expression. These results demonstrated that CTNNB1, BMP4, and NOG, but not SOST, may contribute to the pathogenesis of CH, AS, and RA.
Insights
Gene expression of CTNNB1, BMP4, and NOG in peripheral blood mononuclear cells (PBMCs) may indicate condylar hyperplasia (CH) pathogenesis. These findings differentiate CH and ankylosing spondylitis (AS) from rheumatoid arthritis (RA) by CTNNB1 levels.
Area of Science:
- Molecular biology
- Genetics
- Immunology
Background:
- Bone morphogenetic proteins (BMPs) and wingless (Wnt) signaling pathways regulate bone metabolism.
- Sclerostin and noggin are key antagonists in bone metabolism.
- Understanding gene expression in inflammatory bone diseases is crucial.
Purpose of the Study:
- To evaluate transcript levels of CTNNB1, SOST, BMP4, and NOG genes in peripheral blood mononuclear cells (PBMCs).
- To compare gene expression in patients with condylar hyperplasia (CH) against rheumatoid arthritis (RA), ankylosing spondylitis (AS), and healthy controls.
- To identify potential molecular markers for CH pathogenesis.
Main Methods:
- Peripheral blood mononuclear cells (PBMCs) were isolated from 10 patients each with CH, AS, RA, and 10 healthy controls.
- Quantitative analysis of CTNNB1, SOST, BMP4, and NOG messenger RNAs (mRNAs) was performed using SYBR Green real-time polymerase chain reaction (PCR).
Main Results:
- CTNNB1 expression was significantly upregulated in CH and AS patients compared to healthy individuals and RA patients.
- BMP4 expression was significantly downregulated in AS, CH, and RA patients compared to healthy controls.
- NOG expression was downregulated in CH and RA patients compared to controls, while SOST expression showed no significant difference between groups.
- Upregulated CTNNB1 expression distinguished CH and AS patients from RA patients.
Conclusions:
- CTNNB1, BMP4, and NOG gene expression may play a role in the pathogenesis of CH, AS, and RA.
- SOST expression does not appear to be significantly involved in the pathogenesis of these conditions.
- Specific gene expression patterns in PBMCs could serve as biomarkers for differentiating these bone-related diseases.
