Increased bone morphogenetic protein receptor type 2 expression may enhance osteoblast differentiation in ankylosing spondylitis

BMPR2 is a transmembrane receptor that binds to signaling molecules called bone morphogenetic proteins (BMPs). It belongs to the TGF-beta receptor superfamily and is specifically involved in the regulation of bone morphogenesis. According to a recent article published in the Journal of Rheumatic Diseases, BMPR2 may play an integral role in the advancement of ankylosing spondylitis (AS) through the mediation of bone morphogenetic protein 2 (BMP2). 

Dr. Jo and colleagues, a team of Korean researchers, obtained the data of facet joints from 14 patients who were diagnosed according to the modified New York criteria and 10 healthy controls (HC). The study findings demonstrated that BMPR2 expression was higher in AS-osteoprogenitor (OP)s than in HC-OPs through RNA-sequencing analysis. The results were further validated through the observation of increased BMPR2 expression in facet joint tissues affected by AS and its derived OPs, both at the messenger RNA and protein levels. Furthermore, primary AS-OPs exhibited a greater response to osteogenic differentiation induced by BMP2 and a higher capacity for smad1/5/8-induced RUNX2 expression compared to HCs. 

BMPs are proteins that can trigger a series of events leading to the formation of endochondral bone. They serve as growth factors, morphogens, and cytokines. During this critical developmental process, progenitor cells differentiate into chondrocytes, which establish a cartilage framework that gradually transforms into hypertrophic cells, representing their final differentiation state. Studies have demonstrated a correlation between elevated levels of BMP2 in the bloodstream and proinflammatory cytokines, increased bone formation activity, and the progression of AS in patients. 

The present study findings suggest that BMPR2 is highly expressed in AS-OPs, with a pronounced inclination towards osteoblast differentiation and bone-forming activity regulated by smad1/5/8-RUNX2 in response to BMP2 stimulation. These findings can provide valuable insights into the pathogenesis of AS and suggest the potential for new rational therapies for clinical AS. However, it is essential to note that further large cohort and clinical studies are necessary to validate the current findings. 

References 

  1. Jo S, Lee SH, Jeon C, Jo HR, Ko E, Whangbo M, et al. Elevated BMPR2 expression amplifies osteoblast differentiation in ankylosing spondylitis. J Rheum Dis. 2023 Oct 1;30(4):243–50.  
  1. Carter S, Braem K, Lories RJ. The role of bone morphogenetic proteins in ankylosing spondylitis. Ther Adv Musculoskelet Dis. 2012 Aug;4(4):293–9.  

 

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