Distinctive Expression of Bone Metabolism-related Genes between PBMCs from Condylar Hyperplasia, Rheumatoid Arthritis, and Ankylosing Spondylitis Patients

• Main Authors: Reza Amirzargar, Gholamreza Shirani, Shokoufeh Raisian, Maryam Davoudi, Saeed Aslani, Shiva Poursani, Shaghayegh Khanmohammadi, Mahdi Mahmoudi, Mohammad Bayat
• Format: Article
• Language: English
• Published: Tehran University of Medical Sciences 2020-10-01
• Series: Iranian Journal of Allergy, Asthma and Immunology
• Subjects: Ankylosing spondylitis; Bone morphogenetic proteins; Rheumatoid ‎arthritis
• Online Access: https://ijaai.tums.ac.ir/index.php/ijaai/article/view/2807

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.