Abstract
Pentraxin 3 (PTX3) is a glycoprotein belonging to the humoral arm of innate immunity that participates in the body’s defence mechanisms against infectious diseases. It has recently been defined as a multifunctional protein, given its involvement in numerous physiological and pathological processes, as well as in the pathogenesis of age-related diseases such as osteoporosis. Based on this evidence, the aim of our study was to investigate the possible role of PTX3 in both the osteoblastic differentiation and calcification process: to this end, primary osteoblast cultures from control and osteoporotic patients were incubated with human recombinant PTX3 (hrPTX3) for 72 h. Standard osteinduction treatment, consisting of β-glycerophosphate, dexamethasone and ascorbic acid, was used as control. Our results showed that treatment with hrPTX3, as well as with the osteogenic cocktail, induced cell differentiation towards the osteoblastic lineage. We also observed that the treatment not only promoted an increase in cell proliferation, but also the formation of calcification-like structures, especially in primary cultures from osteoporotic patients. In conclusion, the results reported here suggest the involvement of PTX3 in osteogenic differentiation, highlighting its osteoinductive capacity, like the standard osteoinduction treatment. Therefore, this study opens new and exciting perspectives about the possible role of PTX3 as biomarker and therapeutic agent for osteoporosis.
Highlights
Introduction published maps and institutional affilIn the early 1990s, pentraxin 3 (PTX3), the prototype of long pentraxin, was first identified
PTX3 is a molecule known for its involvement in modulating the mechanisms of innate immunity, which come into play to protect the body from infectious diseases [6,7,8]
We have shown that treatment with anti-PTX3 antibody significantly affects the behavior of osteoblasts, which lose the morphological and molecular characteristics of mature osteoblasts, acquiring a fibroblast-like phenotype and significantly reducing receptor activator of nuclear factor kappa-B ligand (RANKL) and Runt-Related Transcription
Summary
In the early 1990s, pentraxin 3 (PTX3), the prototype of long pentraxin, was first identified. It is a soluble pattern recognition molecule (PRM), released by myeloid lineage cells (dendritic cells, macrophages and monocytes) and stromal cells (epithelial cells, smooth muscle cells, chondrocytes and fibroblasts) in response to primary pro-inflammatory cytokines, damage-associated molecular patterns (DAMPs), agonists of Toll-like receptors (TLRs), microbial components or intact microorganisms [1,2,3,4,5]. Numerous studies have shown over the years that Ptx3-deficient mice are more susceptible to viral, bacterial and fungal infections [9,10,11]. In vivo and in vitro studies have shown that PTX3 binds iations
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