ArticleBMC musculoskeletal disorders2016
The influence of calcitonin gene-related peptide on markers of bone metabolism in MG-63 osteoblast-like cells co-cultured with THP-1 macrophage-like cells under virtually osteolytic conditions.
Article in BMC musculoskeletal disorders, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Effects of Thermal Environment on Bone Microenvironment: A Narrative Review.International journal of molecular sciences · 2025Review
- Crosstalk between Bone and Nerves within Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Use of in vitro bone models to screen for altered bone metabolism, osteopathies, and fracture healing: challenges of complex models.Archives of toxicology · 2020Review
- A Comparison of Osteoblast and Osteoclast In Vitro Co-Culture Models and Their Translation for Preclinical Drug Testing Applications.International journal of molecular sciences · 2020Review
- The Effects of Biomaterial Implant Wear Debris on Osteoblasts.Frontiers in cell and developmental biology · 2020Review
- Acetyl-11-keto-β-boswellic acid attenuates titanium particle-induced osteogenic inhibition via activation of the GSK-3β/β-catenin signaling pathway.Theranostics · 2019Article
- A study on the prevention and treatment of murine calvarial inflammatory osteolysis induced by ultra-high-molecular-weight polyethylene particles with neomangiferin.Experimental and therapeutic medicine · 2018Article
- Glucagon-like peptide 2 decreases osteoclasts by stimulating apoptosis dependent on nitric oxide synthase.Cell proliferation · 2018Article
- The Impact of Metal Ion Exposure on the Cellular Behavior of Human Osteoblasts and PBMCs: In Vitro Analyses of Osteolytic Processes.Materials (Basel, Switzerland) · 2017Article
- αCGRP Regulates Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells Through ERK1/2 and p38 MAPK Signaling Pathways.Cell transplantationArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe neuropeptide calcitonin gene-related peptide (CGRP) has been described to have an inhibitory effect on endotoxin- and wear particle-induced inflammation in the early stages of periprosthetic osteolysis. In the present study, the crosstalk between immune cells and osteoblasts in osteolytic conditions treated with CGRP has been analyzed to evaluate whether the anti-inflammatory properties of the peptide also have a beneficial, i.e. an anti-resorptive and osteo-anabolic impact on bone metabolism.
methodsMG-63 osteoblast-like cells were co-cultured with THP-1 macrophage-like cells stimulated with either ultra-high molecular weight polyethylene (UHMWPE) particles or different concentrations of bacterial lipopolysaccharides (LPS) and simultaneously treated with CGRP. Inflammation was monitored in terms of measuring the levels of tumor necrosis factor (TNF)-α secretion. Furthermore, the production of the osteoblast markers osteoprotegerin (OPG), receptor activator of nuclear factor κB ligand (RANKL), alkaline phosphatase (ALP) and osteopontin (OPN) was quantified. Also, ALP enzymatic activity was measured.
resultsStimulation of co-cultured THP-1 macrophages with either high levels of LPS or UHMWPE induced the secretion of TNF-α which could be inhibited by CGRP to a great extent. However, no remarkable changes in the OPG/RANKL ratio or bone ALP activity were observed. Interestingly, OPN was exclusively produced by THP-1 cells, thus acting as a marker of inflammation. In addition, TNF-α production in THP-1 single cell cultures was found to be considerably higher than in co-cultured cells.
conclusionsIn the co-culture system used in the present study, no obvious relation between inflammation, its mitigation by CGRP, and the modulation of bone metabolism became evident. Nonetheless, the results suggest that during the onset of periprosthetic osteolysis the focus might lie on the modulation of inflammatory reactions. Possibly, implant-related inflammation might merely have an impact on osteoclast differentiation rather than on the regulation of osteoblast activity.
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